πŸ‘€ Chao Lin

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Also published as: Ai-Hsuan Lin, Aifu Lin, Ailong Lin, Aiping Lin, Aizhen Lin, Alexander Lin, Alexander P Lin, Ann Lin, Bei Lin, Bencheng Lin, Bi-Yun Lin, Biaoyang Lin, Bichun Lin, Bihua Lin, Bin Lin, Binbin Lin, Bing-Biao Lin, Bing-Jin Lin, Bing-Xue Lin, Bing-Yao Lin, Bingbing Lin, Bingqi Lin, Bo Lin, Bo-Wen Lin, Bode Lin, Bonnie Lin, Boxu Lin, Brian Leei Lin, Brian Lin, Bridget M Lin, C H Lin, C T Lin, C Y Lin, Cai-Xia Lin, Caiyu Lin, Chang Lin, Chang-Ching A Lin, Changchun Lin, Changpo Lin, Chao-Chieh Lin, Chao-Feng Lin, Chao-Hsiung Lin, Chaohui Lin, Charles P Lin, Chen Lin, Chen-Yong Lin, Cheng Lin, Cheng-Chieh Lin, Cheng-Li Lin, Cheng-Yen Lin, Chengping Lin, Chengqi Lin, Chengyuan Lin, Chenquan Lin, Chi-Hung Lin, Chi-Shiuan Lin, Chi-Ying Lin, Chia-Chin Lin, Chia-Hao Lin, Chia-Ho Lin, Chia-Hsin Lin, Chia-Hung Lin, Chia-Liang Lin, Chia-Yu Lin, Chiao-Huang Lin, Chiao-Mei Lin, Chien-Ju Lin, Chien-Wei Lin, Chien-Yu Lin, Chih-Chun Lin, Chih-Hsun Lin, Chih-Ming Lin, Chih-Pei Lin, Chih-Yu Lin, Chii-Mei Lin, Chin-Hsien Lin, Chin-Sheng Lin, Chin-Yu Lin, Ching-Hung Lin, Ching-Yih Lin, Ching-Yu Lin, Chingju Lin, Cho-Hao Lin, Chuan Lin, Chuan-Chao Lin, Chun Lin, Chun-Lin Lin, Chun-Mao Lin, Chung-Hsien Lin, Chung-Ming Lin, Chunhua Lin, Chunming Lin, Chyuan-Sheng Lin, Cindy Lin, Cong Lin, Cuei-Jyuan Lin, Cui-Jun Lin, Cuilan Lin, Dafeng Lin, Daiqiong Lin, Dan Lin, Dan-Yu Lin, Daniel W Lin, Danyu Lin, Dao-Chao Lin, De-Chen Lin, Ding Lin, Dong Lin, Dong-Tsamn Lin, Dongmei Lin, Dongru Lin, Dongxin Lin, Dongzi Lin, Douglas I Lin, Eugene Lin, F Lin, Fan Lin, Fan-Li Lin, Fang Lin, Fangrui Lin, Fangyu Lin, Fangzhao Lin, Fei Lin, Fen Lin, Feng Lin, Feng-Chang Lin, Feng-Ming Lin, Feng-Yen Lin, Foxiang Lin, Fu Sheng Lin, Fujun Lin, Gang Lin, Ge Lin, Grace Lin, Guan-Bo Lin, Guang-Yao Lin, Guangzheng Lin, Gufa Lin, Guihu Lin, Guimei Lin, Guo-Wang Lin, Guofu Lin, Guoqiang Lin, Guowen Lin, H G Lin, H R Lin, Hai Lin, Haibiao Lin, Haimiao Lin, Haipeng Lin, Haitong Lin, Haiyan Lin, Han Lin, Han-Huei Lin, Hang Lin, Hang-Yan Lin, Hanyu Lin, Hao Lin, Hao-Yu Lin, Haochang Lin, Haocheng Lin, Haodong Lin, Haoyi Lin, Haoyu Lin, He Lin, Heng Lin, Heng-Huei Lin, Henghui Lin, Hening Lin, Hong Lin, Hongcheng Lin, Hongchun Lin, Honghuang Lin, Hongkun Lin, Hongsheng Lin, Hongyan Lin, Hsiao-Yun Lin, Hsien-Chih Lin, Hsin-Ti Lin, Hsing-Pei Lin, Hsiu-Chu Lin, Hua Lin, Huanhuan Lin, Hui Lin, Hui-Hsuan Lin, Hui-Ju Lin, Hui-Kuan Lin, Hui-Ping Lin, Hui-Ru Lin, Hui-Yan Lin, Hui-Yi Lin, Huijuan Lin, Huilan Lin, Huimei Lin, Huisheng Lin, Hung-Chih Lin, Hung-Ju Lin, Hung-Jung Lin, I-Ching Lin, I-Jung Lin, I-Ling Lin, Jake Lin, James A Lin, Jamie S Lin, Jane-Ming Lin, Jeng-Feng Lin, Jia Lin, Jia-Bin Lin, Jia-Feng Lin, Jia-Li Lin, Jia-Qi Lin, Jiabin Lin, Jiacheng Lin, Jiaheng Lin, Jiahui Lin, Jiajing Lin, Jiali Lin, Jiamao Lin, Jiamei Lin, Jian-Yu Lin, JianMin Lin, Jiandie D Lin, Jiandie Lin, Jianfei Lin, Jiang Lin, Jianhao Lin, Jianhua Lin, Jianhui Lin, Jianjian Lin, Jiantao Lin, Jianwei Lin, Jianyin Lin, Jiaqi Lin, Jiaqian Lin, Jiaquan Lin, Jiarui Lin, Jiatong Lin, Jiayang Lin, Jiayi Lin, Jiayuh Lin, Jie Lin, Jie Ming Lin, Jieye Lin, Jieying Lin, Jijin Lin, Jim Jr-Min Lin, Jin Lin, Jin'e Lin, Jin-Ru Lin, Jinchuan Lin, Jing Lin, Jing-Ping Lin, Jing-Ying Lin, Jing-Yu Lin, Jinghan Lin, Jingmei Lin, Jingyu Lin, Jingyuan Lin, Jinlong Lin, Jinxiu Lin, Jinzhong Lin, Jiu Lin, Jiuann-Huey Ivy Lin, Jiunn-Lee Lin, Jiyan Lin, Jo-Yu Lin, Joanne Lin, Johnson Lin, Jue Lin, Juin-Han Lin, Jun-Ming Lin, Junjian Lin, Junnan Lin, Junyi Lin, Kai Lin, Kai-Hsin Lin, Kai-Min Lin, Kai-Yan Lin, Kai-Yen Lin, Kang Lin, Kashuai Lin, Katia Lin, Ke Lin, Ke-Shin Lin, Kejian Lin, Keng-Hung Lin, Kim Y Lin, Kimberly Y Lin, Kongying Lin, Kuan-Hung Lin, Kuang Lin, L Lin, L Y Lin, Lanyan Lin, Le-Hang Lin, Lei Lin, Leilei Lin, Lezhen Lin, Li An Lin, Li Lin, Li-An Lin, Li-Ching Lin, Li-E Lin, Li-Fen Lin, Li-Ling Lin, Li-Rong Lin, Li-Song Lin, Lian-Yu Lin, Liang-Chun Lin, Liang-Tzung Lin, Lihao Lin, Lijin Lin, Liling Lin, Limei Lin, Lin Lin, Ling Lin, Ling-Li Lin, Liping Lin, Lisong Lin, Liwen Lin, Lizhong Lin, Lizhu Lin, Long Lin, Long-Yau Lin, Lu Lin, Luping Lin, M Lin, Manjie Lin, Mao-Shin Lin, Mao-Tsun Lin, Mary Grace Lin, Mei-Chi Lin, Meifang Lin, Meizhen Lin, Meng-Fei Lin, Meng-Wei Lin, Mengsha Lin, Mengxin Lin, Mengyao Lin, Miao Lin, Miao-Chong Joy Lin, Min Lin, Min-Huan Lin, Min-Jie Lin, Min-Rou Lin, Ming-Der Lin, Ming-Hong Lin, Ming-Huei Lin, Ming-Tai Lin, Ming-Wei Lin, Mingkuan Lin, Mingmei Lin, Mingqun Lin, Mingrui Lin, Mingxing Lin, Mingying Lin, Monica Lin, Nan Lin, Nancy U Lin, Nianwei Lin, Ning Lin, Ning-Ning Lin, Ningning Lin, Pei Lin, Pei-Chin Lin, Pei-Lin Lin, Pei-Yi Lin, Peijia Lin, Peng Lin, Peng-Chan Lin, Pengfei Lin, Penghui Lin, Ping Lin, Pingping Lin, Po-Han Lin, Qi Lin, Qian Lin, Qianmeng Lin, Qiannan Lin, Qiao Lin, Qiao-Hong Lin, Qiaoxuan Lin, Qichang Lin, Qin Lin, Qing Lin, Qinghua Lin, Qingling Lin, Qingqing Lin, Qingxiang Lin, Qinlu Lin, Qiong Lin, Qiongfen Lin, Qitai Lin, Qiuling Lin, Qu Lin, Quan-Zhen Lin, R-I Lin, Raozhou Lin, Renjing Lin, Richard Z Lin, Rong Lin, Ronghai Lin, Rongjie Lin, Ru Lin, Rui Lin, Ruifan Lin, Ruilang Lin, Ruiyi Lin, Rutao Lin, S C Lin, S K Lin, S L Lin, S Lin, S Y Lin, S-J Lin, Sen Lin, Sen-Qing Lin, Sha Lin, Shan Lin, Shanyi Lin, Shanyun Lin, Shaowei Lin, Sharon Lin, Sheldon S Lin, Sheng Lin, Sheng-Cai Lin, Sheng-Che Lin, Sheng-Jia Lin, Sheng-Wei Lin, Sheng-Xiang Lin, Shengjie Lin, Shi Lin, Shiaw-Yih Lin, Shibo Lin, Shih-Cherng Lin, Shih-Chieh Lin, Shih-Fan Lin, Shih-Wei Lin, Shih-Yi Lin, Shihui Lin, Shijie Lin, Shin-Yu Lin, Shing-Jong Lin, Shinian Lin, Shinn-Zong Lin, Shinne-Ren Lin, Shiow J Lin, Shiow Lin, Shiping Lin, Shiru Lin, Shiya Lin, Shiyu Lin, Shu Lin, Shu-Chun Lin, Shu-Hui Lin, Shu-Rung Lin, Shu-Wha Lin, Shuai Lin, Shuaijun Lin, Shuan-Pei Lin, Shuhai Lin, Shujuan Lin, Shun-Guo Lin, Shuo Lin, Shuqian Lin, Shyr-Yi Lin, Si-Xian Lin, Simin Lin, Simon Lin, Siong-Chi Lin, Sisi Lin, Siying Lin, Song-Shu Lin, Songyi Lin, Sophia Lin, Spencer Lin, Su-Fang Lin, Sue-Jane Lin, Sufen Lin, Suyang Lin, Suzhen Lin, Ta-Hsien Lin, Tai-Chi Lin, Tao Lin, Tianfeng Lin, Tianxin Lin, Tien-Huang Lin, Tim Lin, Ting Lin, Ting-Hsu Lin, Ting-ting Lin, Tingsheng Lin, Tingting Lin, Tse-I Lin, Tsu-Kung Lin, Tsung-Hsien Lin, Tsung-Shih Lin, Tung-Yi Lin, Tzu-Chien Lin, Vicky Lin, Wan-Wan Lin, Wan-Yu Lin, Wan-Yun Lin, Wanhui Lin, Wanjun Lin, Wei Lin, Wei-De Lin, Wei-Ling Lin, Wei-Ting Lin, Wei-Tso Lin, Wei-Wen Lin, Wei-Xiong Lin, Wei-Yin Lin, Wei-Yu Lin, WeiHao Lin, Weichun Lin, Weiji Lin, Weilong Lin, Weimin Lin, Weiqiang Lin, Wen-Jun Lin, Wen-Jye Lin, Wenjian Lin, Wenming Lin, Wenxin Lin, X J Lin, X Lin, Xi Lin, Xian-Bin Lin, Xian-Zi Lin, Xianchai Lin, Xiandong Lin, Xiang-Quan Lin, Xiangquan Lin, Xiangwu Lin, Xiangyang Lin, Xianke Lin, Xianmei Lin, Xianzhi Lin, Xianzi Lin, Xiao Lin, Xiao-Chun Lin, Xiao-long Lin, Xiaodi Lin, Xiaohan Lin, Xiaohong Lin, Xiaohui Lin, Xiaojing Lin, Xiaoling Lin, Xiaolong Lin, Xiaomin Lin, Xiaoqing Lin, Xiaowei Lin, Xiaoyan Lin, Xiaoyang Lin, Xiaoyi Lin, Xiaoyu Lin, Xiaozeng Lin, Xihong Lin, Xin Lin, Xin-Mei Lin, Xin-Xiu Lin, Xinchun Lin, Xinda Lin, Xing Lin, Xingguang Lin, Xinhua Lin, Xinrong Lin, Xinshi Lin, Xinxin Lin, Xinyao Lin, Xiu-Ru Lin, Xixiao Lin, Xu Lin, Xue Lin, Xue-Jing Lin, Xuefei Lin, Xuehua Lin, Xuejing Lin, Xuelian Lin, Xuemei Lin, Xuewan Lin, Xuyao Lin, Xuyong Lin, Y C Lin, Y Lin, Y M Lin, Ya-Hui Lin, Ya-Lin Lin, Ya-Qiu Lin, Ya-Tin Lin, Yan Lin, Yan-Ling Lin, Yancheng Lin, Yang Lin, Yang-Hsiang Lin, Yani Lin, Yanjun Lin, Yanke Lin, Yanni Lin, Yanqin Lin, Yanxia Lin, Yanzhu Lin, Yao Lin, Yao-Ping Lin, Yaohui Lin, Yaqiu Lin, Ye Lin, Yen-Chun Lin, Yen-Feng Lin, Yen-Hong Lin, Yen-Kuang Lin, Yen-Lin Lin, Yen-Shu Lin, Yen-Yi Lin, Yi Lin, Yi-An Lin, Yi-Chen Lin, Yi-Haou Lin, Yi-Hsiung Lin, Yi-Hsuan Lin, Yi-Hui Lin, Yi-Jang Lin, Yi-Ling Lin, Yi-Nan Lin, Yi-Tzu Lin, Yi-Wen Lin, Yichuan Lin, Yifei Lin, Yifeng Lin, Yihui Lin, Yilong Lin, Yina Lin, Ying Lin, Ying-Chao Lin, Ying-Hsi Lin, Yingnan Lin, Yingni Lin, Yingting Lin, Yingzhong Lin, Yiqi Lin, Yone Kawe Lin, Yong Lin, Yong-Shiang Lin, Yongbin Lin, Yongyao Lin, You Bin Lin, Youcheng Lin, Youwen Lin, Yu Lin, Yu-Chen Lin, Yu-Ching Lin, Yu-Cui Lin, Yu-Fen Lin, Yu-Hsiang Lin, Yu-Hsuan Lin, Yu-Hui Lin, Yu-Lin Lin, Yu-Ling Lin, Yu-Shan Lin, Yu-Sheng Lin, Yu-Wen Lin, Yuan Lin, Yuan-Feng Lin, Yuansheng Lin, Yubi Lin, Yuchen Lin, Yue-Jun Lin, Yueh-Min Lin, Yuezhi Lin, Yuhao Lin, Yuki Lin, Yuli Lin, Yun-Chi Lin, Yun-Lu Lin, Yun-Zhi Lin, Yunfeng Lin, Yung-Chieh Lin, Yung-Ming Lin, Yuntao Lin, Yunting Lin, Yutong Lin, Yuxi Lin, Yuxiang Lin, Yuxin Lin, Yuyuan Lin, Yuzheng Lin, Z Lin, Zaihong Lin, Ze-Shiang Lin, Zebin Lin, Zesen Lin, Zesi Lin, Zexing Lin, Zhangyu Lin, Zhao Lin, Zhaohua Lin, Zhaotong Lin, Zheguang Lin, Zhekai Lin, Zhen Lin, Zheng Lin, Zhengfang Lin, Zhengjie Lin, Zhenhu Lin, Zhenjia Lin, Zhenming Lin, Zhenping Lin, Zhenzhen Lin, Zheshen Lin, Zhi-Heng Lin, Zhi-Hu Lin, Zhi-ming Lin, Zhibin Lin, Zhichao Lin, Zhicheng Lin, Zhien Lin, Zhijian Lin, Zhijie Lin, Zhiqi Lin, Zhixian Lin, Zhixiong Lin, Zhiyi Lin, Zhiying Lin, Zhiyong Lin, Zhong-Hua Lin, Zhongdong Lin, Zhonghua Lin, Zhongjie Lin, Zhongqiu Lin, Zhongxiao Lin, Zhoumeng Lin, Zhuojia Lin, Zi-Han Lin, Zien Lin, Zihan Lin, Ziqiang Lin, Ziwei Lin, Zixian Lin, Zongyun Lin
articles

Precision medicine in diabetes prediction: Exploring a subgroup-specific biomarker strategy for risk stratification.

I-Weng Yen, Szu-Chi Chen, Chia-Hung Lin +9 more Β· 2025 Β· Journal of diabetes investigation Β· Blackwell Publishing Β· added 2026-04-24
The early detection of high-risk individuals is crucial to delay and reduce the incidence of type 2 diabetes. In this study, we aimed to explore the performance of a novel subgroup-specific biomarker Show more
The early detection of high-risk individuals is crucial to delay and reduce the incidence of type 2 diabetes. In this study, we aimed to explore the performance of a novel subgroup-specific biomarker strategy in the prediction of incident diabetes. In the Taiwan Lifestyle Cohort Study, adult subjects without diabetes were included and followed for the incidence of diabetes in 2006-2019. The biomarkers measured included blood secretogranin III (SCG3), vascular adhesion protein-1 (VAP-1), fibrinogen-like protein 1 (FGL1), angiopoietin-like protein 6 (ANGPTL6), and angiopoietin-like protein 4 (ANGPTL4). Among the 1,287 subjects, 12.2% developed diabetes during a 6 year follow-up. Blood VAP-1 was significantly associated with incident diabetes in the overall population (HR = 0.724, P < 0.05), participants under 65 years old (HR = 0.685, P < 0.05), those with a BMI of β‰₯24 kg/m Gender- and BMI-specific biomarker strategy can improve the prediction of incident diabetes. A subgroup-specific biomarker strategy is a novel approach in the prediction of incident diabetes. Show less
πŸ“„ PDF DOI: 10.1111/jdi.14311
ANGPTL4

Combination of Plasma Pharmacochemistry, RNA-Seq, and Molecular Docking Strategies to Reveal the Mechanism of the Alkaloid Fraction of

Yuan Cai, Rong Huang, Tianfeng Lin +6 more Β· 2025 Β· Molecules (Basel, Switzerland) Β· MDPI Β· added 2026-04-24
πŸ“„ PDF DOI: 10.3390/molecules30183727
APOA4

Silencing the chicken seven transmembrane (Ch-7TM) receptor leads to apoptosis in chicken mononuclear phagocytes.

Jia-Ling Yang, Long-Huw Lee, Hsing-Chieh Wu +3 more Β· 2025 Β· Developmental and comparative immunology Β· Elsevier Β· added 2026-04-24
The seven-transmembrane (7TM) receptors are the largest superfamily of cell-surface receptors and are involved in various physiological processes of vertebrate species. In our previous study, a new ch Show more
The seven-transmembrane (7TM) receptors are the largest superfamily of cell-surface receptors and are involved in various physiological processes of vertebrate species. In our previous study, a new chicken 7TM receptor (Ch-7TM) was discovered in mononuclear phagocytes (MNPs) derived from chicken peripheral blood mononuclear cells (PBMCs). To explore the functions of Ch-7TM, RNA interference (RNAi) was used to silence the Ch-7TM messenger RNA (mRNA) of MNPs, using small interfering RNA (siRNA) designed with BLOCK-iTβ„’ RNAi Designer. Herein we demonstrated that silencing of the Ch-7TM mRNA induced apoptosis of MNPs, suggesting that Ch-7TM contributed to the survival of MNPs. Moreover, chicken sera could inhibit the Ch-7TM-silencing-induced apoptosis in MNPs. The survival factor presented in fraction 16 (F16) of chicken sera was highly protective against the Ch-7TM-silencing-induced apoptosis in MNPs. The proteins from F16 were identified as vitamin D-binding protein (DBP) and apolipoprotein A-IV (ApoA-IV), which might be potential candidates for survival factors. The protective effect of vitamin D and ApoA-IV indicated that Ch-7TM might involve the intracellular oxidation-reduction balance, although more evidence is needed to confirm this function. The siRNA screening serves as an excellent model for studying the functions of chicken MNPs receptors. Show less
no PDF DOI: 10.1016/j.dci.2025.105423
APOA4

Cigarette smoke-induced PPAR signaling dysregulation accelerates Alzheimer's disease pathogenesis and cognitive decline in 5xFAD mice.

Yunqi Xie, Haochen Wang, Yajie Zhang +5 more Β· 2025 Β· Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association Β· Elsevier Β· added 2026-04-24
Smoking is harmful to health. Cigarette smoke (CS) contains a variety of toxic substances. Studies have found that nicotine, tar, polycyclic aromatic hydrocarbons, etc. in CS can pass through the bloo Show more
Smoking is harmful to health. Cigarette smoke (CS) contains a variety of toxic substances. Studies have found that nicotine, tar, polycyclic aromatic hydrocarbons, etc. in CS can pass through the blood-brain barrier and enter the brain to exert their effects. Moreover, some existing studies have pointed out that CS exposure is closely related to the accelerated pathology of Alzheimer's disease (AD). Transgenic mice with the five familial AD mutations (5xFAD), which are 1-month-old, were used for chronic CS exposure for 100 days. Subsequently, cognitive function and behavioral changes were evaluated through morris water maze and new object recognition tests. The acceleration of pathological changes due to CS exposure was assessed by HE, Tunel and AΞ² immunohistochemical staining. Differential expression proteins and metabolites were screened through hippocampal proteomics and metabolomics analyses. Finally, the expression levels of key proteins were verified by Western blot. Compared with unexposed 5xFAD mice, the behavioral results of mice showed that FAD mice after CS exposure exhibited poorer cognitive abilities, with longer latencies in the Morris water maze, and decreased time spent and entries in the target quadrant. The results of pathological sections indicated that the total nuclei density in the DG and CA3 regions of the hippocampus of 5xFAD mice decreased significantly after chronic CS exposure, the number of TUNEL-positive cells increased, and the expression of AΞ²42 increased. Multi - omics analysis revealed that CS exposure up - regulated the expression of 46 proteins and down - regulated the expression of 80 proteins in the hippocampus of 5xFAD mice, and caused changes in 92 metabolites. Analysis of the correlation between differential proteins and differential metabolites revealed six key cross-node proteins: Kng1, Hbb-b1, Fabp3, Apoa1, Ilk, and Apoa4. CS exposure may accelerate pathological changes and cognitive impairment in 5xFAD mice by affecting energy metabolism through the PPAR signaling pathway. Show less
no PDF DOI: 10.1016/j.fct.2025.115596
APOA4

Apolipoprotein A-IV regulates coagulation and ischemic stroke by potentiating activated protein C.

Musan Yan, Yuewei Wang, Liyuan Niu +13 more Β· 2025 Β· Journal of thrombosis and haemostasis : JTH Β· Elsevier Β· added 2026-04-24
Inflammation is crucial in regulating coagulation and hemostasis. While prior research shows that apolipoprotein A-IV (ApoA-IV) has anti-inflammatory and antiplatelet effects, its specific impact on c Show more
Inflammation is crucial in regulating coagulation and hemostasis. While prior research shows that apolipoprotein A-IV (ApoA-IV) has anti-inflammatory and antiplatelet effects, its specific impact on coagulation remains unclear. To investigate the effects of ApoA-IV on the coagulation system, including its interactions with potential targets and the underlying mechanisms. Plasma ApoA-IV levels in deep vein thrombosis patients were tested by enzyme-linked immunosorbent assay. The effects of ApoA-IV on coagulation were assessed through thromboelastography. Potential interactions and mechanisms were analyzed using surface plasmon resonance and AlphaFold 3. Mice bleeding and stroke models were employed to evaluate the effects on hemostasis and thrombosis. ApoA-IV levels were reduced in deep vein thrombosis patients and correlated with increased thrombotic risk. Thromboelastography showed that ApoA-IV treatment delayed clot reaction and kinetic times while decreasing thrombus generation angle and maximum amplitude, highlighting its crucial role in inhibiting coagulation and platelet aggregation. We identified ApoA-IV as a functional activator of activated protein C (APC), with critical interactions occurring at residues 144 to 148 within the exosite loop of the APC protease domain. In animal models, anti-ApoA-IV antibody administration shortened bleeding time but exacerbated ischemic stroke outcomes. Notably, inhibitory peptide HE5, which inhibits ApoA-IV-APC interaction, effectively counteracted the anticoagulant activity of ApoA-IV. These findings establish ApoA-IV as a pivotal regulator of coagulation and hemostasis, primarily through enhancing APC activity. This research advances our understanding of the interplay between inflammation, lipid metabolism, and thrombosis, offering insights for developing novel antithrombotic therapies. Show less
no PDF DOI: 10.1016/j.jtha.2025.05.033
APOA4

Potential of CETP inhibition in treating dyslipidemia in systemic lupus erythematosus: Novel and comprehensive evidence from clinical studies and Mendelian randomization.

Yihong Gan, Yilin Zhang, Jingqun Liu +10 more Β· 2025 Β· International immunopharmacology Β· Elsevier Β· added 2026-04-24
Cardiovascular diseases from abnormal lipid metabolism significantly increase mortality in systemic lupus erythematosus (SLE). The causal link between dyslipidemia and SLE is unclear. Lipid metabolism Show more
Cardiovascular diseases from abnormal lipid metabolism significantly increase mortality in systemic lupus erythematosus (SLE). The causal link between dyslipidemia and SLE is unclear. Lipid metabolism in patients with SLE was evaluated based on clinical data from 511 patients with SLE and 706 healthy individuals. Bidirectional Mendelian randomization (MR) was employed to assess causal links between 179 plasma lipid metabolites, lipid-lowering drug targets, and SLE risk. Genetic instruments from GWAS and eQTL data were used to evaluate CETP and APOA4 effects. Peripheral blood CETP and apolipoprotein levels in SLE patients were validated via ELISA. SLE patients exhibited reduced HDL-C (PΒ <Β 0.0001), APOA1 (PΒ <Β 0.0001), and APOA4 (PΒ <Β 0.0001), alongside elevated triglycerides (TG, PΒ <Β 0.0001), APOC3, APOD, and APOF. MR identified three lipid metabolites-PC(18:2β‚‚β‚€:4), TG(56:6), and TG(58:7)-as causal factors for SLE (PΒ <Β 2.79E-5). CETP inhibition significantly reduced SLE risk via HDL-C modulation (ORΒ =Β 0.72, PΒ =Β 3.38E-08) and influenced LDL-C, TG, and apolipoproteins. Clinical validation confirmed elevated CETP and reduced APOA4 in SLE, correlating with disease activity. APOA4 activation showed protective effects, while PCSK9 inhibition lacked relevance. Bidirectional Mendelian randomization analyses confirmed dyslipidemia as a causal antecedent to SLE, with no evidence of reverse causation. A variety of MR analyses and clinical validation indicated that targeting HDL-C regulation offers significant advantages for managing dyslipidemia in patients with SLE, with CETP identified as the optimal pharmacological target. Show less
no PDF DOI: 10.1016/j.intimp.2025.114736
APOA4

Cholesteryl ester transfer protein activity correlates inversely with apolipoprotein A5 levels.

Yi Wen, Hongxia Li, Sydney Smith +9 more Β· 2025 Β· Journal of clinical lipidology Β· Elsevier Β· added 2026-04-24
Cholesteryl ester transfer protein (CETP) mediates the exchange of triglycerides (TG) from apolipoprotein B (ApoB)-containing lipoproteins to high-density lipoproteins (HDL) and the reciprocal exchang Show more
Cholesteryl ester transfer protein (CETP) mediates the exchange of triglycerides (TG) from apolipoprotein B (ApoB)-containing lipoproteins to high-density lipoproteins (HDL) and the reciprocal exchange of cholesterol (C) from HDL to ApoB-containing lipoproteins. CETP inhibition increases HDL-C and decreases low-density lipoprotein cholesterol (LDL-C) while modestly decreasing TG. Considering that CETP inhibitors block removal of TG from TG-rich lipoproteins (TRL), it is interesting that CETP inhibition decreases TG concentrations. TG levels are largely regulated by lipoprotein lipase (LPL), the enzyme primarily responsible for hydrolyzing TG. The angiopoietin-like 3/8 complex (ANGPTL3/8) is the most potent circulating LPL inhibitor, while the TG-lowering apolipoprotein A5 (ApoA5) acts by suppressing ANGPTL3/8-mediated LPL inhibition. To better understand CETP biology, we studied the effects of CETP overexpression and CETP inhibition on the levels of ANGPTL3/8 and ApoA5 in circulation using dedicated immunoassays. CETP-overexpressing transgenic mice had increased TG and normal ANGPTL3/8 levels but manifested dramatically reduced ApoA5 concentrations. Administration of the CETP inhibitor evacetrapib had no effect on ANGPTL3/8 levels in CETP-overexpressing mice or in humans. However, evacetrapib administration increased ApoA5 concentrations in both species. In human subjects, evacetrapib treatment increased circulating ApoA5 levels in the late-stage ACCELERATE and ACCENTUATE studies by 160.1% and 204.7%, respectively. Our results uncover a previously unrecognized link between CETP and ApoA5 by showing that CETP overexpression reduces ApoA5 levels while CETP inhibition increases ApoA5 concentrations. Show less
no PDF DOI: 10.1016/j.jacl.2025.06.008
APOA5

Gene clusters linked to insulin resistance identified in a genome-wide study of the Taiwan Biobank population.

Eugene Lin, Yu-Ting Yan, Mu-Hong Chen +3 more Β· 2025 Β· Nature communications Β· Nature Β· added 2026-04-24
This pioneering genome-wide association study examined surrogate markers for insulin resistance (IR) in 147,880 Taiwanese individuals using data from the Taiwan Biobank. The study focused on two IR su Show more
This pioneering genome-wide association study examined surrogate markers for insulin resistance (IR) in 147,880 Taiwanese individuals using data from the Taiwan Biobank. The study focused on two IR surrogate markers: the triglyceride to high-density lipoprotein cholesterol (TG:HDL-C) ratio and the TyG index (the product of fasting plasma glucose and triglycerides). We identified genome-wide significance loci within four gene clusters: GCKR, MLXIPL, APOA5, and APOC1, uncovering 197 genes associated with IR. Transcriptome-wide association analysis revealed significant associations between these clusters and TyG, primarily in adipose tissue. Gene ontology analysis highlighted pathways related to Alzheimer's disease, glucose homeostasis, insulin resistance, and lipoprotein dynamics. The study identified sex-specific genes associated with TyG. Polygenic risk score analysis linked both IR markers to gout and hyperlipidemia. Our findings elucidate the complex relationships between IR surrogate markers, genetic predisposition, and disease phenotypes in the Taiwanese population, contributing valuable insights to the field of metabolic research. Show less
πŸ“„ PDF DOI: 10.1038/s41467-025-58506-x
APOA5

Genetic Variants in Severe Hypertriglyceridemia Among Taiwanese Participantsγ€€- Insights From Genome-Wide Association and Whole-Exome Sequencing Analyses.

Hsien-Yu Fan, Ming-Chieh Tsai, Chih-Jun Lai +9 more Β· 2025 Β· Circulation journal : official journal of the Japanese Circulation Society Β· added 2026-04-24
There are limited data on the use of whole-exome sequencing (WES) to diagnose severe hypertriglyceridemia. Our aim was to identify candidate genes linked to triglyceride levels via a genome-wide assoc Show more
There are limited data on the use of whole-exome sequencing (WES) to diagnose severe hypertriglyceridemia. Our aim was to identify candidate genes linked to triglyceride levels via a genome-wide association study (GWAS) and to recruit participants with severe hypertriglyceridemia for WES to assess allelic variants in the candidate genes. A GWAS was conducted involving 120,140 participants to identify lead loci associated with blood triglyceride levels. Following the identification of these lead loci, WES was performed on DNA samples from 29 participants with hypertriglyceridemia whose triglyceride levels exceeded 800 mg/dL to assess variations in the corresponding genes. In the GWAS of 120,140 participants, the apolipoprotein A5 (APOA5) locus on chromosome 11 showed the strongest association with blood triglyceride levels (lead single nucleotide polymorphism [SNP] rs2075291; P=3.07Γ—10 Our study confirms the role of known genetic loci in triglyceride metabolism and hypertriglyceridemia while uncovering novel loci, offering new perspectives on lipid regulation and potential avenues for therapeutic advancements. Show less
no PDF DOI: 10.1253/circj.CJ-24-0491
APOA5

Meta-Analysis and Machine Learning Prediction of Protein Corona Composition across Nanoparticle Systems in Biological Media.

Alexa Canchola, Keyuan Li, Kunpeng Chen +12 more Β· 2025 Β· ACS nano Β· ACS Publications Β· added 2026-04-24
A comprehensive understanding of protein corona (PC) composition is critical for engineering nanoparticles (NPs) with optimal safety and therapeutic performance, because the PC governs NP pharmacokine Show more
A comprehensive understanding of protein corona (PC) composition is critical for engineering nanoparticles (NPs) with optimal safety and therapeutic performance, because the PC governs NP pharmacokinetics, biodistribution, and cellular interactions. Yet systematic analyses are hampered by the absence of standardized, richly annotated data sets. Here, we introduce the Protein Corona Database (PC-DB), which compiles data from 83 studies (2000-2024) and integrates 817 NP formulations with quantitative profiles of 2497 adsorbed proteins. The PC-DB exposes pronounced heterogeneity in NP materials (metal 28.8%, silica 22.8%, lipid-based 14.8%), surface modifications, sizes (1-1400 nm), and ΞΆ-potentials (-70 to +70 mV). Subsequent meta-analysis shows that silica, polystyrene, and lipid-based NPs smaller than 100 nm with moderately negative to neutral ΞΆ-potentials preferentially bind the lipoproteins APOE and APOB-100, which are linked to receptor-mediated uptake and enhanced delivery efficiency. In contrast, metal and metal-oxide NPs carrying highly negative surface charge enrich complement component C3, indicating a greater likelihood of immune recognition and clearance. Interpretable machine learning models (LightGBM and XGBoost; ROC-AUC > 0.85) confirm NP size, ΞΆ-potential, and incubation time as the most influential predictors of protein adsorption. These results delineate how physicochemical parameters dictate PC composition and illustrate the power of predictive modeling to guide rational NP design. Show less
πŸ“„ PDF DOI: 10.1021/acsnano.5c08608
APOB

Identification of novel biomarkers involved in oral squamous cell carcinoma by whole transcriptome sequencing and bioinformatics analysis.

Hongliang Du, Zhenze Wang, Mengyi Qi +4 more Β· 2025 Β· Cancer cell international Β· BioMed Central Β· added 2026-04-24
Oral squamous cell carcinoma (OSCC) is among the most common malignant tumors in the oral and maxillofacial regions, characterized by high drug resistance and poor treatment outcomes. This underscores Show more
Oral squamous cell carcinoma (OSCC) is among the most common malignant tumors in the oral and maxillofacial regions, characterized by high drug resistance and poor treatment outcomes. This underscores the urgent need to identify novel biomarkers for OSCC. Differentially expressed messenger RNAs (mRNAs), microRNAs (miRNAs), and long non-coding RNAs (lncRNAs) (DE-mRNAs, DE-miRNAs, and DE-lncRNAs) between primary and control groups, as well as metastatic and primary groups, were identified using whole transcriptome sequencing data. Candidate OSCC genes were derived from DE-mRNAs. Potential biomarkers were then identified using five algorithms from CytoHubba. Biomarkers were validated via univariate Cox regression and Kaplan-Meier (K-M) survival analysis. Additional analyses included subcellular localization, mutation analysis, and Gene Set Enrichment Analysis (GSEA). Key drugs for OSCC treatment were also identified. Quantitative real time polymerase chain reaction (qRT-PCR) and immunohistochemistry were employed to verify the expression levels of key biomarkers. A total of 304 candidate genes were identified, with 29 potential biomarkers selected by five algorithms. ANPEP, APOB, GLP1R, and SI exhibited significant survival differences in the K-M curves, establishing them as OSCC biomarkers. These biomarkers were predominantly localized in the cytoplasm, with SI and APOB showing the highest mutation susceptibility. Enrichment analysis revealed that the 'interferon-gamma response'biological function was co-enriched by ANPEP, APOB, and SI. Furthermore, BIBW2992 (afatinib) and PF.02341066 (crizotinib) were most strongly correlated with the biomarkers, suggesting their potential as key drugs for OSCC treatment. Additionally, the findings were validated by qRT-PCR and immunohistochemical analyses, and the results were consistent with the RNA-seq data. ANPEP, APOB, GLP1R, and SI were identified as potential OSCC biomarkers, offering valuable insights for further research and therapeutic development. Show less
πŸ“„ PDF DOI: 10.1186/s12935-025-03913-9
APOB

Treatment with orforglipron, an oral glucagon like peptide-1 receptor agonist, is associated with improvements of CV risk biomarkers in participants with type 2 diabetes or obesity without diabetes.

Sean Wharton, Julio Rosenstock, Manige Konige +7 more Β· 2025 Β· Cardiovascular diabetology Β· BioMed Central Β· added 2026-04-24
Orforglipron, a novel oral, non-peptide glucagon like peptide-1 (GLP-1) receptor agonist, has demonstrated efficacy in improving body weight reduction and glycemic control. However, its potential bene Show more
Orforglipron, a novel oral, non-peptide glucagon like peptide-1 (GLP-1) receptor agonist, has demonstrated efficacy in improving body weight reduction and glycemic control. However, its potential benefits in improving cardiovascular (CV) risk factors have yet to be determined. We assessed the effect of orforglipron in participants with type 2 diabetes (T2D) and/or overweight or obesity on blood pressure, lipid, and inflammatory biomarkers associated with risk for major adverse cardiovascular events. Using data from participants with available samples from Phase 2 trials of orforglipron in participants with T2D (N = 361) or with overweight or obesity without diabetes mellitus (N = 234), we performed an exploratory analysis of changes in CV risk markers. For the T2D study, participants mean age 59Β years, 40% were assigned female at birth with a mean HbA Significant placebo-adjusted decreases from baseline in blood pressure, low-density lipoprotein (LDL) cholesterol, triglycerides, ApoB, ApoC3, and hsCRP were observed following orforglipron treatment in participants with T2D and/or overweight or obesity. In both studies, improvements in blood pressure, lipid parameters, and most of the evaluated biomarkers were of similar magnitude after treatment with 12Β mg orforglipron as with 24, 36, and 45Β mg. Orforglipron treatment was associated with beneficial changes in CV risk markers in participants with T2D and in participants with overweight/obesity without T2D. (Clinicaltrials.gov: NCT05048719, NCT05051579). Show less
πŸ“„ PDF DOI: 10.1186/s12933-025-02781-x
APOB

Proteomic profiles screening identified novel exosomal protein biomarkers for diagnosis of lung cancer.

Weiyan Feng, Ying Lin, Ling Zhang +1 more Β· 2025 Β· Clinical proteomics Β· BioMed Central Β· added 2026-04-24
Exosomes play important role in biological functions, including both normal and disease process. Multiple cell types can secret exosomes, which act as message carriers. Increased evidences reveal that Show more
Exosomes play important role in biological functions, including both normal and disease process. Multiple cell types can secret exosomes, which act as message carriers. Increased evidences reveal that exosomes are promising diagnosis biomarkers in malignant tumors. In this study, we enrolled 78 participants, including 20 lung adenocarcinoma (LUAD), 18 lung squamous carcinoma (LUSC), 20 lung benign diseases (LUBN) and 20 healthy controls (NL) and we performed parallel reaction-monitoring (PRM)-mass spectrometry to screening the proteomic variation by label free analysis in exosomes from all groups, which has been widely used to quantify and detect target proteins. Total 14 protein were identified as candidate biomarkers, complement components C9, apolipoprotein B (APOB), filamin A (FLNA), guanine nucleotide binding protein G subunit 2 (GNB2), fermitin family homolog 3 (FERMT3) showed significantly differentiation in total lung cancer (LUAD and LUSC together), we then obtained combination analysis of 5 proteins and the area under the curve (AUC), sensitivity (SN) and specificity (SP) were 63.0%, 65.0%, and 75.0%, respectively, in comparison to NL group. And the LUAD combination panel, peroxiredoxin 6 (PRDX6), integrin alpha-IIb (ITGA2B) and hemoglobin subunit delta (HBD) revealed AUC was 95.0%, SN was 90.0% and SP was 95.0% in comparison to NL controls. In LUSC analysis, combination analysis of fibronectin 1 (FN1), pregnancy zone protein (PZP) and complement C1q tumor necrosis factor related protein 3 (C1QTNF3) showed that AUC was 88.1%, SN was 75.0%, SP was 100% in paralleled with NL group. Finally C9, FLNA, PZP were overexpressed in lung cancer H1299 and A549 cell lines and the results indicated that C9 acted as oncogenic role by increasing proliferation, migration and invasion of lung cancer cells, while FLNA and PZP played tumor-suppression by inhibition biological functions of lung cancer cells. Taken together, our study revealed multiple exosomal proteins which could be applied as candidate biomarkers in diagnosis of lung cancer. Show less
πŸ“„ PDF DOI: 10.1186/s12014-025-09535-7
APOB

Relationship of Apolipoprotein B to Aortic Aneurysm: Frailty Index as a Partial Mediator - a Mendelian Randomization Study.

Tongxue Zhang, Yajing Li, Xiaoyu Liu +8 more Β· 2025 Β· Kardiologiia Β· added 2026-04-24
Aim Β  Β Aortic aneurysm is characterized by localized expansion and damage to the vessel wall. While apolipoprotein B (ApoB) has been linked to atherosclerosis, its causal relationship with aortic aneu Show more
Aim Β  Β Aortic aneurysm is characterized by localized expansion and damage to the vessel wall. While apolipoprotein B (ApoB) has been linked to atherosclerosis, its causal relationship with aortic aneurysm remains unclear. This study used a Mendelian randomization (MR) approach to explore the causal relationships between ApoB, aortic aneurysm, and potential mediators.Material and methods Β  Β Single nucleotide polymorphism (SNP) data related to ApoB, apolipoprotein A1 (ApoA1), triglycerides, frailty index, and aortic aneurysm were obtained from large-scale genome-wide association studies. MR analysis was conducted to evaluate causal relationships, using inverse variance weighting (IVW) as the primary statistical method. Additionally, we assessed whether the frailty index mediates the relationship between ApoB and aortic aneurysm.Results Β  Β Univariate MR analysis revealed that ApoB is significantly associated with aortic aneurysm (IVW odds ratio (OR) = 1.443, 95 % confidence interval (CI) = 1.273-1.637, p < 0.001). Multivariable MR (MVMR) analysis, adjusted for ApoA1 and triglycerides, confirmed these results. In mediation analysis, the frailty index was found to partially mediate the effect of ApoB on aortic aneurysm (mediation contribution: 20.1 %-23.1 %). The ORs for ApoB and the frailty index with respect to aortic aneurysm were 1.325 (95 % CI = 1.168-1.505) and 4.188 (95 % CI = 1.859-9.435), respectively.Conclusion Β  Β ApoB has a causal relationship with aortic aneurysm, with the frailty index acting as a partial mediator in this pathway. Show less
no PDF DOI: 10.18087/cardio.2025.2.n2796
APOB

Single-cell transcriptomic atlas of the chicken cecum reveals cellular responses and state shifts during Eimeria tenella infection.

Jun-Hao Tu, Bo-Gong Liu, Bing-Jin Lin +7 more Β· 2025 Β· BMC genomics Β· BioMed Central Β· added 2026-04-24
Eimeria tenella (E. tenella) infection is a major cause of coccidiosis in chickens, leading to significant economic losses in the poultry industry due to its impact on the cecum. This study presents a Show more
Eimeria tenella (E. tenella) infection is a major cause of coccidiosis in chickens, leading to significant economic losses in the poultry industry due to its impact on the cecum. This study presents a comprehensive single-cell atlas of the chicken cecal epithelium by generating 7,394 cells using 10X Genomics single-cell RNA sequencing (scRNA-seq). We identified 13 distinct cell types, including key immune and epithelial populations, and characterized their gene expression profiles and cell-cell communication networks. Integration of this single-cell data with bulk RNA-seq data from E. tenella-infected chickens revealed significant alterations in cell type composition and state, particularly a marked decrease in APOB Show less
πŸ“„ PDF DOI: 10.1186/s12864-025-11302-9
APOB

Body Fat Distribution and Ectopic Fat Accumulation as Mediator of Diabetogenic Action of Lipid-Modifying Drugs: A Mediation Mendelian Randomization Study.

Yuanlong Hu, Xinhai Cui, Mengkai Lu +11 more Β· 2025 Β· Mayo Clinic proceedings Β· Elsevier Β· added 2026-04-24
To investigate the causal relationship between various lipid-modifying drugs and new-onset diabetes, as well as the mediators contributing to this relationship. Mediation Mendelian randomization was p Show more
To investigate the causal relationship between various lipid-modifying drugs and new-onset diabetes, as well as the mediators contributing to this relationship. Mediation Mendelian randomization was performed to investigate the causal effect of lipid-modifying drug targets on type 2 diabetes (T2D) outcomes and the proportion of this association that is mediated through ectopic fat accumulation traits. Specific sets of variants in or near genes that encode 11 lipid-modifying drug targets (LDLR, HMGCR, NPC1L1, PCSK9, APOB, ABCG5/ABCG8, LPL, PPARA, ANGPTL3, APOC3, and CETP; for expansion of gene symbols, use search tool at www.genenames.org) were extracted. Random effects inverse variance weighted were performed to evaluate the causal effects among outcomes. Mediation analyses were performed to identify the mediators of the association between lipid-modifying drugs and T2D. The study was conducted from November 10, 2023, to April 2, 2024 RESULTS: The genetic mimicry of HMGCR and APOB inhibition was associated with an increased T2D risk, whereas the genetic mimicry of LPL enhancement was linked to a lower T2D risk. Gluteofemoral adipose tissue volume was a mediator for explaining 9.52% (P=.002), 16.90% (P=.03), and 10.50% (P=.003) of the total effect of HMGCR, APOB, and LPL on T2D susceptibility, respectively. Liver fat was a mediator for explaining 21.12% (P=.005), 12.28% (P=.03), and 9.84% (P=.005) of the total effect of HMGCR, APOB, and LPL on T2D susceptibility, respectively. Our findings support the hypothesis that liver fat and gluteofemoral adipose tissue play a mediating role in the prodiabetic effects of HMGCR and APOB inhibition, as well as in the antidiabetic effects of LPL enhancement. Show less
no PDF DOI: 10.1016/j.mayocp.2024.10.018
APOB

Validation of the role of apolipoproteins in coronary artery disease patients with impaired kidney function for prognosis: a prospective cohort study in China.

Zixiang Ye, Enmin Xie, Zhangyu Lin +5 more Β· 2025 Β· Nutrition journal Β· BioMed Central Β· added 2026-04-24
This study aims to evaluate the relationship between apolipoproteins (ApoA1, ApoB, and the ApoB/A1 ratio) and the incidence of major adverse cardiovascular events (MACE) in patients with coronary arte Show more
This study aims to evaluate the relationship between apolipoproteins (ApoA1, ApoB, and the ApoB/A1 ratio) and the incidence of major adverse cardiovascular events (MACE) in patients with coronary artery disease (CAD) and impaired kidney function, assessing their potential role in secondary prevention. A prospective cohort of 1,640 patients with impaired kidney function who underwent percutaneous coronary intervention in China was analyzed. Patients were categorized based on the measurements of ApoA1, ApoB, and ApoB/A1 ratio. MACE, defined as a composite of all-cause mortality, cardiovascular death, nonfatal myocardial infarctions, strokes, and unplanned revascularizations, was tracked post-procedure, with statistical analyses including Kaplan-Meier survival curves and Cox regression models to identify associations with apolipoproteins. Subgroup analyses according to kidney function were conducted. During a median follow-up of 3.1Β years, 324 MACE events were observed. Multivariable Cox regression analyses illustrated higher levels of ApoB and the ApoB/A1 ratio were significantly associated with increased MACE incidence (adjusted HR [95%CI] 1.668[1.044-2.666]; adjusted HR [95%CI] 2.231[1.409-3.533], respectively), while lower ApoA1 levels correlated with a higher risk (adjusted HR [95%CI] 0.505[0.326-0.782]). ROC curve analyses indicated comparable predictive performances to traditional risk factors like LDL cholesterol. Subgroup analysis revealed that the above association was not statistically significant in the moderate-to-severe renal impairment CAD patients (eGFR < 45Β mL/min/1.73 m Our findings illustrate that apolipoproteins, specifically ApoA1 and ApoB, along with their ratio, are significant predictors of major adverse cardiovascular events in CAD patients with impaired kidney function. These results emphasize the need for incorporating apolipoprotein measurements in secondary prevention strategies for this high-risk population. Show less
πŸ“„ PDF DOI: 10.1186/s12937-025-01078-9
APOB

High-Density Lipoprotein Lipid and Protein Cargo and Cholesterol Efflux Capacity Before and After Bariatric Surgery.

Sohail Zahid, Florencia Schlamp, Michael A Gildea +8 more Β· 2025 Β· Arteriosclerosis, thrombosis, and vascular biology Β· added 2026-04-24
Cholesterol efflux capacity (CEC) of HDL (high-density lipoprotein) is inversely associated with incident cardiovascular events, independent of HDL cholesterol. Obesity is characterized by low HDL cho Show more
Cholesterol efflux capacity (CEC) of HDL (high-density lipoprotein) is inversely associated with incident cardiovascular events, independent of HDL cholesterol. Obesity is characterized by low HDL cholesterol and impaired HDL function, such as CEC. Bariatric surgery, including Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy (SG), broadly leads to improved cardiovascular outcomes, but impacts on risk factors differ by procedure, with greater improvements in weight loss, blood pressure, and glycemic control after RYGB, but greater improvements in HDL cholesterol and CEC levels after SG. This study sought to determine effects of RYGB and SG on HDL protein and lipid cargo and investigate associations with CEC changes. We prospectively studied nondiabetic, premenopausal Hispanic women with severe obesity not using lipid medications undergoing RYGB (n=31) or SG (n=36). Anthropometric measurements and blood sampling were obtained before and at 6 and 12 months after surgery. HDL was isolated from plasma, and quantitative proteomic and lipidomic assessments were performed with LC-MS/MS (liquid chromatography with tandem mass spectrometry). CEC was assessed ex vivo using apoB-depleted serum. Participants experienced similar, significant weight loss over 12 months following bariatric surgery (38.0Β±10.4 kg) regardless of the procedure. Relative quantities of 47 proteins (34 increased, 13 decreased) and 150 lipids (71 increased, 79 decreased) carried on HDL were significantly altered following either surgical procedure. Proteins with similar aggregate response patterns were clustered into 15 groups (5 increased, 5 decreased, 5 minimal change) and lipids with similar aggregate responses into 25 groups (7 increased, 11 decreased, 7 minimal change). Network mediation analyses suggested that changes in 4 protein and 2 lipid clusters mediated changes in ABCA1 (ATP-binding cassette transporter A1) CEC and that 1 lipid cluster mediated changes in non-ABCA1 CEC. The protein and lipid clusters that mediated changes in CEC were distinct between SG and RYGB. Bariatric surgery produces substantial changes in HDL lipid and protein cargo, and specific changes may mediate changes in HDL function in CEC. Further study of these mechanisms may lead to improved interventions to reduce cardiovascular risk in patients with obesity. Show less
πŸ“„ PDF DOI: 10.1161/ATVBAHA.124.321686
APOB

A whole-animal phenotypic drug screen identifies suppressors of atherogenic lipoproteins.

Daniel J Kelpsch, Liyun Zhang, James H Thierer +9 more Β· 2025 Β· bioRxiv : the preprint server for biology Β· Cold Spring Harbor Laboratory Β· added 2026-04-24
Lipoproteins are essential for lipid transport in all bilaterians. A single Apolipoprotein B (ApoB) molecule is the inseparable structural scaffold of each ApoB-containing lipoprotein (B-lps), which a Show more
Lipoproteins are essential for lipid transport in all bilaterians. A single Apolipoprotein B (ApoB) molecule is the inseparable structural scaffold of each ApoB-containing lipoprotein (B-lps), which are responsible for transporting lipids to peripheral tissues. The cellular mechanisms that regulate ApoB and B-lp production, secretion, transport, and degradation remain to be fully defined. In humans, elevated levels of vascular B-lps play a causative role in cardiovascular disease. Previously, we have detailed that human B-lp biology is remarkably conserved in the zebrafish using an Show less
πŸ“„ PDF DOI: 10.1101/2024.11.14.623618
APOB

J-shaped association between apolipoprotein B and CV outcomes in statin-treated patients with chronic coronary syndrome.

Jining He, Zhangyu Lin, Chenxi Song +5 more Β· 2025 Β· Revista espanola de cardiologia (English ed.) Β· Elsevier Β· added 2026-04-24
The association between apolipoprotein B (apoB) and residual cardiovascular (CV) risk in patients with chronic coronary syndrome (CCS) remains unclear. We aimed to investigate the association between Show more
The association between apolipoprotein B (apoB) and residual cardiovascular (CV) risk in patients with chronic coronary syndrome (CCS) remains unclear. We aimed to investigate the association between apoB levels and CV outcomes in statin-treated CCS patients. We enrolled 8641 statin-treated CCS patients at Fuwai Hospital. The patients were divided into 5 groups based on to apoB quintiles (Q1 to Q5). The primary endpoint was 3-year CV events, including CV death, nonfatal myocardial infarction, and nonfatal stroke. During a median follow-up of 3.17 years, there were 232 (2.7%) CV events. After multivariable adjustment, a restricted cubic spline illustrated a J-shaped relationship between apoB levels and 3-year CV events, with the risk remaining flat until apoB levels exceeded 0.73g/L, after which the risk increased (nonlinear P <.05). Kaplan-Meier curves showed the lowest CV event rate in the Q3 group (0.68-0.78g/L). Compared with the Q3 group, multivariable Cox regression models revealed that both low (Q1, ≀0.57g/L) and high (Q5, >0.93g/L) apoB levels were associated with an increased risk of major adverse cardiac events (all P <.05). Notably, patients with low apoB levels (Q1) had the highest risk of CV death (HR, 2.44; 95%CI, 1.17-5.08). Our analysis indicates that both low and high levels of apoB are associated with elevated CV risk, with the risk being particularly pronounced at higher levels (> 0.73g/L). Show less
no PDF DOI: 10.1016/j.rec.2024.08.004
APOB

Copper metabolism-related biomarkers and therapeutic targets for diabetic nephropathy.

Qiaofang Yan, Yuanyuan Du, Fei Huang +9 more Β· 2025 Β· PeerJ Β· added 2026-04-24
Diabetic nephropathy (DN) is the most intractable complication of diabetes. Despite decades of research, accurate diagnostic markers and effective therapeutic drugs are still elusive. Abnormal copper Show more
Diabetic nephropathy (DN) is the most intractable complication of diabetes. Despite decades of research, accurate diagnostic markers and effective therapeutic drugs are still elusive. Abnormal copper metabolism is also implicated in diabetes and its complications. This study aims to identify copper metabolism-related biomarkers and potential drugs for DN. DN datasets and copper metabolism-related genes (CMGs) were obtained from Gene Expression Omnibus (GEO) and GeneCards. Differentially expressed CMGs (DE-CMGs) were identified using the limma package and the Venn algorithm. Functional enrichment analysis and protein-protein interaction (PPI) network were performed to identify candidate hub genes. The single gene with an area under the receiver operating characteristic (ROC) curve > 0.7 was identified as a potential diagnostic biomarker of DN. Finally, these biomarkers were validated by quantitative real-time polymerase chain reaction (qRT-PCR) in high-glucose-treated human proximal tubular (HK-2) cells. These validated hub genes were used to construct a combined prediction model, confirmed by additional GSE30528 and GSE30529 datasets. The correlation analysis between the expression level of the hub genes and the estimated glomerular filtration rate (eGFR) was carried out. Additionally, immune cell infiltration and potential target drugs were investigated for these biomarkers. Five hub genes associated with copper metabolism, namely CD36, CCL2, CASP3, LPL, and APOC3, were identified as biomarkers for the early diagnosis of DN. Utilizing multiple biomarkers enhanced diagnostic accuracy and specificity. CD36, CCL2, and CASP3 correlated negatively with eGFR levels, while LPL and APOC3 correlated positively. Additionally, these hub genes were significantly linked to various immune cell types, including macrophages M1 and M2, T cells, gamma delta resting dendritic cells, neutrophils, and NK cells. Furthermore, 15 agents targeting these biomarkers were retrieved from the DrugBank database. Our study identified key genes possibly related to copper metabolism in the pathological mechanism of DN that could serve as novel targets for the diagnosis and therapy of DN. Show less
πŸ“„ PDF DOI: 10.7717/peerj.20468
APOC3

The association of lipids and novel non-statin lipid-lowering drug target with osteoporosis: evidence from genetic correlations and Mendelian randomization.

Qingcong Zheng, Rongjie Lin, Du Wang +2 more Β· 2025 Β· BMC musculoskeletal disorders Β· BioMed Central Β· added 2026-04-24
It remains controversial whether lipids affect osteoporosis (OP) or bone mineral density (BMD), and causality has not been established. This study aimed to investigate the genetic associations between Show more
It remains controversial whether lipids affect osteoporosis (OP) or bone mineral density (BMD), and causality has not been established. This study aimed to investigate the genetic associations between lipids, novel non-statin lipid-lowering drug target genes, and OP and BMD. Mendelian randomization (MR) method was used to explore the genetic associations between 179 lipid species and OP, BMD. Drug-target MR analysis was used to explore the causal associations between angiopoietin-like protein 3 (ANGPTL3) and apolipoprotein C3 (APOC3) inhibitors on BMD. The IVW results with Bonferroni correction indicated that triglyceride (TG) (51:3) (OR = 1.0029; 95% CI: 1.0014-1.0045; P = 0.0002) and TG (56:6) (OR = 1.0021; 95% CI: 1.0008-1.0033; P = 0.0011) were associated with an increased risk of OP; TG (51:2) (OR = 0.9543; 95% CI: 0.9148-0.9954; P = 0.0298) was associated with decreased BMD; and ANGPTL3 inhibitor (OR = 1.1342; 95% CI: 1.0393-1.2290; P = 0.0093) and APOC3 inhibitor (OR = 1.0506; 95% CI: 1.0155-1.0857; P = 0.0058) was associated with increased BMD. MR analysis indicated causal associations between genetically predicted TGs and OP and BMD. Drug-target MR analysis showed that ANGPTL3 and APOC3 have the potential to serve as novel non-statin lipid-lowering drug targets to treat or prevent OP. Show less
πŸ“„ PDF DOI: 10.1186/s12891-024-08160-z
APOC3

Identification of immune-related genes in diagnosing hypercholesterolemia with myocardial infarction through bioinformatics analysis.

Weibin Wu, Zheng Peng, Yi Yu +5 more Β· 2025 Β· Frontiers in immunology Β· Frontiers Β· added 2026-04-24
Increasing evidence suggests that familial hypercholesterolemia (FHC) exacerbates myocardial infarction (MI). This study aimed to identify possible candidate biomarkers for patients with FHC and MI. T Show more
Increasing evidence suggests that familial hypercholesterolemia (FHC) exacerbates myocardial infarction (MI). This study aimed to identify possible candidate biomarkers for patients with FHC and MI. The data were obtained from Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were screened using Limma, while module genes were identified through Weighted Gene Co-expression Network Analysis (WGCNA) in GSE48060. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analysis, protein-protein interaction (PPI) network and CIBERSORT methods were performed to explore the intersection genes. A receiver operating characteristic (ROC) curve were employed to evaluate the diagnostic effectiveness, with validation conducted using datasets GSE61144 and RT-qPCR. The FHC datasets included 656 DEGs, while there were 956 DEGs and 90 module genes in MI datasets. There were 49 overlapping DEGs between FHC and MI, which were associated with immune functions. Additionally, immune infiltration analysis revealed disturbances in immune cell populations. There were 13 candiate hub genes were screen after PPI network analysis. Show less
πŸ“„ PDF DOI: 10.3389/fimmu.2025.1715216
APOE

Disruption of cerebral cholesterol homeostasis by PS-NPs: astrocytic endoplasmic reticulum stress.

Lei Tian, Yizhe Wei, Jianping Ma +10 more Β· 2025 Β· Journal of nanobiotechnology Β· BioMed Central Β· added 2026-04-24
Cholesterol plays a crucial role in regulating synaptic membrane fluidity and ion channels. Due to the blood-brain barrier, cholesterol in the brain is primarily self-synthesized by astrocytes. Howeve Show more
Cholesterol plays a crucial role in regulating synaptic membrane fluidity and ion channels. Due to the blood-brain barrier, cholesterol in the brain is primarily self-synthesized by astrocytes. However, limited research has been conducted on the effects of polystyrene nanoplastic (PS-NPs) on intracranial cholesterol metabolic pathways. In this study, we exposed whole-brain organoids (WBOs) to PS-NPs and identified significant changes in endoplasmic reticulum stress and cholesterol biosynthesis pathways through whole-transcriptome sequencing. To investigate potential mechanisms of altered cholesterol pathways, we constructed a Transwell neuronal-astrocyte co-culture model. Results demonstrated that PS-NPs induced significant endoplasmic reticulum stress in astrocytes, specifically manifested by elevated levels of ATF4 and CHOP, along with increased autophagy indicated by the elevated LC3-II/I ratio. PS-NPs significantly inhibited the AKT/ACLY pathway of cholesterol biosynthesis, leading to marked reductions in acetyl-CoA and cholesterol within astrocytes (P < 0.05). In addition, PS-NPs led to a significant reduction of apolipoprotein APOE, which hindered cholesterol transport and ultimately inhibited synaptin (SYN) formation. In summary, PS-NPs induce endoplasmic reticulum stress and autophagy in astrocytes, impair cholesterol de novo synthesis and apolipoprotein-mediated transport, ultimately inhibiting neuronal synaptogenesis. Furthermore, specific inhibition of ERs restored cholesterol synthesis in astrocytes and neuronal synapses. This study demonstrates that PS-NPs produce neurotoxic effects by affecting cholesterol homeostasis in the brain. Show less
πŸ“„ PDF DOI: 10.1186/s12951-025-03949-z
APOE

Integrating Vascular Aging and Genetic Risk: The Combined Impact of Estimated Pulse Wave Velocity and Genetic Predisposition on Coronary Artery Disease.

Chang Sheng, Rui Zhou, Hongcai Wang +4 more Β· 2025 Β· Journal of the American Heart Association Β· added 2026-04-24
Estimated pulse wave velocity (ePWV), a noninvasive marker of arterial stiffness, reflects vascular aging and has been associated with increased coronary artery disease (CAD) risk. However, the interp Show more
Estimated pulse wave velocity (ePWV), a noninvasive marker of arterial stiffness, reflects vascular aging and has been associated with increased coronary artery disease (CAD) risk. However, the interplay between ePWV and genetic factors, including polygenic risk score (PRS) and apolipoprotein E genotypes, in determining CAD susceptibility remains unclear. We analyzed data from the HRS (Health and Retirement Study), including 5856 participants (4741 White and 1115 Black individuals) without baseline CAD. ePWV was calculated, and genetic risk was assessed using PRS and apolipoprotein E genotyping. Cox proportional hazards models evaluated the associations between ePWV, genetic predisposition, and CAD incidence, with stratified analyses by race and sex. Mediation analyses explored underlying mechanisms. Elevated ePWV (β‰₯10 m/s) was significantly associated with increased CAD risk (hazard ratio [HR], 1.50 [95% CI, 1.25-1.81], Vascular aging and genetic predisposition interact in complex ways to influence CAD risk, with notable variations across racial and sex subgroups. These findings highlight the need for personalized prevention strategies incorporating both vascular health and genetic risk profiling. Show less
πŸ“„ PDF DOI: 10.1161/JAHA.125.042610
APOE

Treadmill exercise ameliorates atherogenesis and vascular inflammation in ApoE

Wenhuang Guo, Jinyun Wang, Zaoshang Chang +6 more Β· 2025 Β· Scientific reports Β· Nature Β· added 2026-04-24
Regular exercise training has been shown to significantly decrease atherosclerosis (AS) related mortality and hospitalization rates. Recent research has identified that circulating exosome-derived mic Show more
Regular exercise training has been shown to significantly decrease atherosclerosis (AS) related mortality and hospitalization rates. Recent research has identified that circulating exosome-derived microRNAs (miRNAs) are closely related to the progression of AS through intercellular communication. But the role of exosome-derived miRNAs in exercise-mediated protection remains to be explored. This study proposes that exercise may ameliorate vascular dysfunction and plaque formation associated with AS by modulating the expression profile of exosomal miRNAs. In this study, ApoE Show less
πŸ“„ PDF DOI: 10.1038/s41598-025-30174-3
APOE

Orally deliverable biomimetic nucleic acid therapies for targeted treatment of atherosclerosis.

Chenwen Li, Yidan Chen, Yuan Li +9 more Β· 2025 Β· Acta pharmaceutica Sinica. B Β· Elsevier Β· added 2026-04-24
Accumulating evidence has demonstrated that nucleic acid-based therapies are promising for atherosclerosis. However, nearly all nucleic acid delivery systems developed for atherosclerosis necessitate Show more
Accumulating evidence has demonstrated that nucleic acid-based therapies are promising for atherosclerosis. However, nearly all nucleic acid delivery systems developed for atherosclerosis necessitate injection, which results in rapid elimination and poor patient compliance. Consequently, oral delivery strategies capable of targeting atherosclerotic plaques are imperative for nucleic acid therapeutics. Herein we report the development of yeast-derived capsules (YCs) packaging an antisense oligonucleotide (AM33) targeting microRNA-33 (miR-33) for the oral treatment of atherosclerosis. YCs provide stability for AM33, preventing its premature release in the gastrointestinal tract. AM33-containing YCs, defined as YAM33, showed high transfection in macrophages, thus promoting cholesterol efflux and inhibiting foam cell formation by regulating the target genes/proteins of miR-33. Orally delivered YAM33 effectively accumulated within atherosclerotic plaques in Show less
πŸ“„ PDF DOI: 10.1016/j.apsb.2025.07.039
APOE

Gene-metabolite interactions in aortic dissection: Insights from metabolic and single-cell analyses.

Chen Yao, Geng Wang, Quanhui Wu +6 more Β· 2025 Β· Medicine Β· added 2026-04-24
Aortic dissection (AD) involves complex interactions among amino acid, glucose, and lipid metabolism, exacerbating aortic inflammation and extracellular matrix (ECM) degradation, coupled with smooth m Show more
Aortic dissection (AD) involves complex interactions among amino acid, glucose, and lipid metabolism, exacerbating aortic inflammation and extracellular matrix (ECM) degradation, coupled with smooth muscle cell (SMC) dysfunction (phenotypic alteration, aging, apoptosis). To explore AD pathogenesis, we integrated single-cell RNA sequencing (scRNA-seq), metabolomics, machine learning, and Mendelian randomization to investigate SMC changes and gene-metabolite interactions. ScRNA-seq data (GSE213740, GSE155468) were analyzed for cell clustering and pseudo-time trajectories via Seurat and Monocle2. Metabolomics (9 samples: 6 AD, 3 controls) and machine learning validated key genes/metabolites, with Mendelian randomization assessing causal links. Nine cell subsets and 2000 variable genes were identified, with SMCs central to AD via cholesterol metabolism. APOE and PLTP were key genes; metabolomics highlighted cholesterol esters (CEs) and triglycerides (TGs) as critical metabolites. Machine learning confirmed APOE/PLTP's high predictive accuracy (AUC: 0.796-0.989). Mendelian randomization linked elevated CEs and TGs to increased AD risk (IVW: Pβ€…=β€….04 and Pβ€…=β€….02, respectively). This study establishes a gene-metabolite network where APOE and PLTP regulate CEs/TGs, influencing SMC function and AD progression, offering potential therapeutic targets. Show less
πŸ“„ PDF DOI: 10.1097/MD.0000000000045846
APOE

Comprehensive single-cell RNA analysis reveals intertumoral microenvironment heterogeneity and hub niche of carcinogenesis in thyroid cancer.

Hao Xu, Junjie Ma, Nanjun Li +6 more Β· 2025 Β· NPJ precision oncology Β· Nature Β· added 2026-04-24
Thyroid cancer, the most common endocrine malignancy, is characterized by a unique and complex tumor microenvironment (TME). To unravel the high tumor heterogeneity and molecular mechanisms driving ca Show more
Thyroid cancer, the most common endocrine malignancy, is characterized by a unique and complex tumor microenvironment (TME). To unravel the high tumor heterogeneity and molecular mechanisms driving cancer progression, we performed single-cell RNA sequencing (scRNA-seq) analysis, enabling a comprehensive exploration of cellular diversity and molecular dynamics at single-cell resolution. We employed Principal Component Analysis (PCA) and Uniform Manifold Approximation and Projection (UMAP) for dimensionality reduction and subsequent identification of cellular clusters. Differential gene expression analysis across subclusters was conducted using the FindAllMarkers function, while the DoHeatmap function was utilized to visualize the distribution of differentially expressed genes. The AUCell algorithm was applied to evaluate pathway enrichment within specific cell subtypes. To decipher cellular communication networks, we integrated the CellChat and NicheNet algorithms, which revealed intricate intercellular signaling interactions. Finally, multiplex immunohistochemistry (mIHC) was performed to validate key cellular interactions identified in silico. By analyzing 405,077 single cells from 50 thyroid cancer samples (including papillary, anaplastic, and metastatic tumors) and 14 normal thyroid tissues, we identified four major cellular subpopulations through unbiased clustering based on gene expression patterns and representative cellular markers. The TME was found to encompass diverse immune, endothelial, and mesenchymal cell subtypes, including novel populations such as CD4 + HSPA1A + T cells. Functional pathway enrichment analysis highlighted the roles of abundant cell types in tumor progression. Cell-cell communication analysis uncovered potential immunotherapeutic targets and revealed critical crosstalk among hub niche cells, including APOE+ macrophages, EMT-like cancer-associated fibroblasts (CAFs), and RBP7+ endothelial cells. These findings were further validated by multiplex immunohistochemistry, confirming the spatial organization and interactions of these cell populations within the TME. Our study provides a comprehensive single-cell transcriptomic atlas of thyroid cancer, offering profound insights into tumor heterogeneity, the functional roles of key niche cells, and potential biomarkers for anticancer therapy. These findings not only enhance our understanding of thyroid cancer biology but also pave the way for the development of novel therapeutic strategies targeting the TME. Show less
πŸ“„ PDF DOI: 10.1038/s41698-025-00924-7
APOE

Role of the Wnt/Ξ²-catenin signaling pathway in the development of HCC.

Bo Lin, Mengsen Li Β· 2025 Β· Frontiers in immunology Β· Frontiers Β· added 2026-04-24
Abnormalities in the Wnt/Ξ²-catenin pathway promote the development of hepatocellular carcinoma (HCC). Mutations in CTNNB1, which encodes Ξ²-catenin, are frequently found in clinical HCC samples, as are Show more
Abnormalities in the Wnt/Ξ²-catenin pathway promote the development of hepatocellular carcinoma (HCC). Mutations in CTNNB1, which encodes Ξ²-catenin, are frequently found in clinical HCC samples, as are loss-of-function mutations in signaling pathway regulators such as axis inhibition protein 1 (Axin1) and adenomatous polyposis coli (APC). The activation of the Wnt/Ξ²-catenin pathway synergizes with other oncogenic signal molecules such as c-Met or glypican-3, contributing to HCC development. Furthermore, Wnt/Ξ²-catenin pathway activation in the tumour microenvironment (TME) leads to cold tumour and resistance to immunotherapy. In this review, we discuss two models of Wnt/Ξ²-catenin signaling activation, role of Wnt/Ξ²-catenin signaling pathway in the development of HCC, the association between Wnt/Ξ²-catenin pathway and tumour angiogenesis, metastasis, and immune escape in the TME, and the targeting of this signaling pathway for HCC treatment. Show less
πŸ“„ PDF DOI: 10.3389/fimmu.2025.1691297
AXIN1