👤 Woo-Jin Kim

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849
Articles
999
Name variants
Also published as: Mi Ok Kim, S Y Kim, Chul-Hong Kim, Do Hyung Kim, Sydney Y Kim, Sung Young Kim, Chongtae Kim, Myung-Sunny Kim, Hyeong-Rok Kim, Miri Kim, Dong Il Kim, Hyeon-Ah Kim, Esther Kim, Ok-Hwa Kim, Juyong B Kim, Joong-Seok Kim, Jong Woo Kim, Saerom Kim, Wondong Kim, Seong-Hyun Kim, Misung Kim, Dong-Ik Kim, Minsuk Kim, Ohn Soon Kim, Sung Han Kim, Sung Tae Kim, Richard Kim, Albert H Kim, Ju Deok Kim, Chong Ae Kim, Hyun-Ji Kim, Yong Kyung Kim, Jisun Kim, Haein Kim, Jeonghan Kim, Hee Jin Kim, Minjae Kim, Hyun Kim, Kyoung Oh Kim, Jiyea Kim, Jun Hoe Kim, Joon Kim, Sunghwan Kim, Bo-Rahm Kim, Namkyoung Kim, Hee Jeong Kim, Kangjoon Kim, Younghoon Kim, Jae Geun Kim, Min Kyeong Kim, Hyeong-Taek Kim, Kevin K Kim, Soeun Kim, Sungup Kim, Jeong Su Kim, Gwang Sik Kim, Anthony S Kim, Ok Jin Kim, Jeongseop Kim, Bo-Eun Kim, Suk-Kyung Kim, Sang Soo Kim, Hae Won Kim, Taeil Kim, Joonyoung R Kim, Kyung-Hee Kim, Hyeyoon Kim, Hyojin Kim, Yangseok Kim, Jong Ho Kim, Chunki Kim, Seokjoong Kim, Mi Ra Kim, Young-Dae Kim, Young Mi Kim, Na-Kuang Kim, Yoon Sook Kim, Byoung Jae Kim, Daham Kim, Mijung Kim, Yu Kyeong Kim, Yong-Lim Kim, Jin-Chul Kim, Chan Wook Kim, Hyeong-Jin Kim, Sang Hyuk Kim, Gibae Kim, Sang Ryong Kim, Jieun Kim, Jongchan Kim, Joseph C Kim, Jun Pyo Kim, Brandon J Kim, Jun-Sik Kim, Ji Eun Kim, Jung-In Kim, Chan-Wha Kim, B-Y Kim, B T Kim, Dahee Kim, Taek-Yeong Kim, Hyunjoon Kim, Young-Saeng Kim, Hyeon Jeong Kim, Hyemin Kim, Shin Kim, Y S Kim, Dan Say Kim, Ji-Dam Kim, Paul T Kim, Kyoung Hoon Kim, Ye-Ri Kim, Hee-Jin Kim, Jason Kim, Youngsin Kim, Hyuk Soon Kim, Seung-Ki Kim, Moon Suk Kim, Young Ju Kim, Yunwoo Kim, J Y Kim, Lia Kim, Soo-Hyun Kim, Byung Jin Kim, You-Sun Kim, Youngsoo Kim, Yunkyung Kim, Meelim Kim, Kye-Seong Kim, Minseon Kim, Hye-Jin Kim, Il-Man Kim, Dong Ha Kim, Soo Yoon Kim, Stuart K Kim, Soo Hyun Kim, Il-Chan Kim, Mi-Na Kim, Yeong-Sang Kim, Eunmi Kim, Taewan Kim, Yun Seok Kim, Kyung Hee Kim, M Kim, Hyun Eun Kim, Eunkyeong Kim, Soee Kim, Young-Im Kim, So-Hee Kim, Hyeong Hoe Kim, Hee Young Kim, Eungseok Kim, Sungyun Kim, Tae-You Kim, Jong-Yeon Kim, Tae Hoon Kim, Sungrae Kim, Eun-Jin Kim, Heejin Kim, Tae Jin Kim, Ju Young Kim, Un-Kyung Kim, Jin Woo Kim, Gu-Hwan Kim, Young-Mi Kim, Dae-Kyum Kim, Tae-Min Kim, Seon-Kyu Kim, Hana Kim, Hye Ran Kim, Yuli Kim, Jung Ho Kim, Edwin H Kim, Grace Kim, Jongho Kim, Soung Jung Kim, Jinsup Kim, Dong-Kyu Kim, Su-Hyeong Kim, Kee-Tae Kim, Nam-Ho Kim, Jin Gyeom Kim, Mi Young Kim, Hyun-Sic Kim, Kyung-Sup Kim, Hyeonwoo Kim, Dong Gwang Kim, Jong-Youn Kim, Doo Yeon Kim, Jong-Il Kim, Soo Whan Kim, Kwang-Eun Kim, Jong-Won Kim, Eung-Gook Kim, Jaehoon Kim, Hyoung Kyu Kim, Hark Kyun Kim, Jonggeol J Kim, Sang Eun Kim, Jeong Kyu Kim, Eun Ji Kim, Youngmi Kim, William Kim, Jiho Kim, Dae In Kim, Dennis Y Kim, Sunghun Kim, Nari Kim, Doyeon Kim, Sang-Min Kim, Myeong-Kyu Kim, Youngsook Kim, Angela H Kim, Hye-Jung Kim, Hyung-Suk Kim, Hang-Rai Kim, Hyoun-Ah Kim, Sung-Wan Kim, Myung-Sun Kim, Mi Kyung Kim, Eun Young Kim, Jinhee Kim, Hyung-Gu Kim, Woo Sik Kim, In Suk Kim, Sung Eun Kim, Yekaterina Kim, Juyoung Kim, Hong-Hee Kim, Hye-Sung Kim, Ji Hyun Kim, Kyung Mee Kim, Sunghak Kim, Dong-Hoon Kim, Yong-Wan Kim, Seul Young Kim, Myoung Ok Kim, Jong-Seok Kim, H Kim, Minsik Kim, Sang-Young Kim, June-Bum Kim, Dong Hyun Kim, Jihoon Kim, Jaegil Kim, Tae Wan Kim, Seonggon Kim, Seongho Kim, Dong Wook Kim, Jun-Hyung Kim, Don-Kyu Kim, Kyung An Kim, Jun Suk Kim, Jung-Lye Kim, Dongkyun Kim, Sung Kyun Kim, Yerin Kim, Seung Woo Kim, Jun W Kim, Eunae Kim, Won Tae Kim, Kyung-Sub Kim, Kang Ho Kim, Chul Hwan Kim, Yong Sig Kim, Hong-Kyu Kim, Go Woon Kim, Peter K Kim, Taeeun Kim, Eunhyun Kim, Min-Sik Kim, Hyejin Kim, Chang-Yub Kim, Kyunggon Kim, Sinai Kim, Jiyeon Kim, Chong Kook Kim, Minkyung Kim, Cecilia E Kim, Jae Seon Kim, Yeon-Jeong Kim, Ha-Neui Kim, Kwan Hyun Kim, Jongwan Kim, Young Hun Kim, Nam Hee Kim, Jong Yeol Kim, Ji-Hoon Kim, Ki Tae Kim, Young-Bum Kim, Hyojung Kim, Woonhee Kim, Minjeong Kim, Sae Hun Kim, Sohee Kim, Jong-Joo Kim, Sangsoo Kim, Yong-Woon Kim, Geun-Young Kim, Jae-Jun Kim, K-K Kim, Jung-Taek Kim, Jeeyoung Kim, Min-Sun Kim, Kwang Pyo Kim, Ngoc-Thanh Kim, Chan-Duck Kim, Hyeon Ho Kim, Soo-Youl Kim, Young Tae Kim, Shi-Mun Kim, Kwang-Pyo Kim, Hee Jong Kim, Minah Kim, Taehyoun Kim, Yonghwan Kim, Won Dong Kim, Su-Jeong Kim, Eunha Kim, Min-Hyun Kim, Kyeongjin Kim, Min Kim, Sung Won Kim, Se-Wha Kim, Myeoung Su Kim, Eonmi Kim, In-Hoo Kim, Nan Young Kim, Myeong Ok Kim, Wootae Kim, In Kyoung Kim, Leen Kim, Doo Yeong Kim, Do-Hyung Kim, Dong-Hyeok Kim, Joonseok Kim, So Yeon Kim, Kwangho Kim, Seok Won Kim, Bo Ri Kim, TaeHyung Kim, Woo Jin Kim, Misun Kim, Serim Kim, Junesun Kim, Young Ree Kim, Choel Kim, Jae Hun Kim, Jin-Soo Kim, Jimi Kim, You-Jin Kim, Goun Kim, Goo-Young Kim, Jong Han Kim, Bongjun Kim, Sun-Joong Kim, Young Ho Kim, Kyung Sup Kim, Young Jin Kim, Scott Y H Kim, Chang Seong Kim, Ryung S Kim, Kellan Kim, Han Gyung Kim, Jae Hoon Kim, Jung-Ha Kim, Jaeyeon Kim, Hyung-Mi Kim, Hye-Young H Kim, Ho Shik Kim, Hwijin Kim, Kyungtae Kim, Ki Kwon Kim, Yongae Kim, Jaemi Kim, Hyun-ju Kim, Tai Kyoung Kim, Se Hyun Kim, Hyeseon Kim, Jin Cheon Kim, Hyung-Ryong Kim, Carla F Kim, Hyunki Kim, Yong-Sik Kim, Joonki Kim, Hyung-Sik Kim, Ah-Ram Kim, Deok Ryong Kim, Hyunyoung Kim, Jung Ki Kim, Yongkang Kim, Brian S Kim, Minchul Kim, Kahye Kim, Jae-Ryong Kim, Heegoo Kim, In Joo Kim, Sung-Jo Kim, Sang Chan Kim, Kyuho Kim, Sunkyu Kim, Beom-Jun Kim, Wanil Kim, Hei Sung Kim, Woojin Scott Kim, Won Jeoung Kim, Jungwoo Kim, Yejin Kim, Kyu-Kwang Kim, Yong-Soo Kim, Yong-Ou Kim, M J Kim, Yoonjung Kim, Chul Hoon Kim, Hyun-Jung Kim, Jae Hyoung Kim, Hyun Joon Kim, Hyun-Jin Kim, Ok-Kyung Kim, Kyungsook Kim, Kyungwon Kim, Jin Kim, Suji Kim, Ok-Hyeon Kim, Jung-Woong Kim, Seoyeon Kim, Kyeong-Min Kim, Sang-Hoon Kim, Hyun Gi Kim, Jooho Kim, Myung-Jin Kim, Eun-Jung Kim, Sangchul Kim, Joori Kim, Min Jung Kim, Jeeho Kim, Jihye Kim, Mi-Young Kim, Choon Ok Kim, Na Yeon Kim, Seong-Ik Kim, Jisu Kim, Dong-Hyun Kim, Myungsuk Kim, Eui Hyun Kim, Won-Tae Kim, Sung Soo Kim, Eun Kim, Hyung Min Kim, Jihyun Kim, Kwang Dong Kim, Suhyun Kim, Elizabeth H Kim, Sang-Gun Kim, Han-Kyul Kim, Yong Deuk Kim, Jong-Seo Kim, Young-Ho Kim, Yoo Ri Kim, Eiru Kim, Ji Yeon Kim, Ki Hyun Kim, Tae Hun Kim, Ae-Jung Kim, Eosu Kim, Cheorl-Ho Kim, TaeYeong Kim, Yeon-Hee Kim, Jae Suk Kim, Richard B Kim, Young-Jin Kim, Deokhoon Kim, Eung Yeop Kim, K-S Kim, Daeseung Kim, Ji Hun Kim, Mi-Sung Kim, Young Woo Kim, Taehyeung Kim, Meesun Kim, Sook Young Kim, Jaewon Kim, In Su Kim, Heebal Kim, Seungsoo Kim, Bong-Jo Kim, Seon Hwa Kim, Luke Y Kim, Jae-Ick Kim, Hwajung Kim, Jisook Kim, Jeffrey J Kim, Kyung Do Kim, Jungeun Kim, Youbin Kim, Jeong-Min Kim, Seokhwi Kim, D-W Kim, Su-Yeon Kim, Jung Hee Kim, Wook Kim, Jun-Mo Kim, Seon Hee Kim, Hong-Gi Kim, Hyun-Young Kim, Young Hwa Kim, Hyung Bum Kim, Dae-Soo Kim, Gitae Kim, Hyun-Yi Kim, Sejoong Kim, Hyungsoo Kim, Hyunmi Kim, June Soo Kim, Gyudong Kim, Rokki Kim, Yong Sook Kim, Young-Il Kim, Jinsu Kim, Woo-Yang Kim, Eunjoon Kim, Woo Kim, Jang-Hee Kim, Won Seok Kim, Seung Tea Kim, Tae Il Kim, Sung-Hou Kim, H S Kim, Suhyung Kim, Jong-Ho Kim, Jong Heon Kim, So Young Kim, Yeonsoo Kim, Jiha Kim, Young-Youn Kim, Hye Yun Kim, Arie Kim, Sun-Hee Kim, Min Wook Kim, Hyung-Jun Kim, Jae Hyun Kim, Sewoon Kim, Jin Seok Kim, Eunju Kim, Yun Hye Kim, Sun-Hong Kim, Soyeong Kim, Sowon Kim, Young Sik Kim, Mi-Hyun Kim, Byung-Gyu Kim, JongKyong Kim, Jin Young Kim, So Ree Kim, Aram Kim, Youn-Jung Kim, Joung Sug Kim, Hail Kim, Eui Jin Kim, Cheol-Su Kim, Ngoc Thanh Kim, Seong-Seop Kim, Ji-Man Kim, Ju-Kon Kim, Soo Wan Kim, Woong-Ki Kim, Ju-Wan Kim, Sunggun Kim, Sun Woong Kim, Jin Kyong Kim, Hoguen Kim, Hyungkuen Kim, Ji Hye Kim, Myoung Hee Kim, Min Ju Kim, Deok-Ho Kim, Woo-Shik Kim, Mina K Kim, Kiyoung Kim, Paul H Kim, Eun-Kyung Kim, Da-Sol Kim, Yeaseul Kim, In Ja Kim, Beomsu Kim, Byungwook Kim, Sun Yeou Kim, Jongmyung Kim, Helen Kim, Sungyeon Kim, Dae-Eun Kim, Jayoun Kim, Jung Dae Kim, Joseph Han Sol Kim, E-S Kim, Boo-Young Kim, Sung-Mi Kim, Dongwoo Kim, Seul-Ki Kim, Hye Jin Kim, Soo Young Kim, Sukjun Kim, Dong Joon Kim, Hyo Jung Kim, Yeseul Kim, Yong Sik Kim, Nam-Eun Kim, Sang-Tae Kim, Hong Sug Kim, Youngjoo Kim, Sun-Gyun Kim, Min-Gon Kim, Young-Woo Kim, Myungshin Kim, Tae Hoen Kim, Soon Hee Kim, Won Kim, Chanhee Kim, Jung Oh Kim, Hyun-Kyong Kim, Jeffrey Kim, Yeonhwa Kim, Yeon Ju Kim, Duck-Hee Kim, Seohyeon Kim, Soon Sun Kim, Jae Bum Kim, Yeul Hong Kim, Juhyun Kim, Chang-Gu Kim, Gwangil Kim, Alison J Kim, Hwa-Jung Kim, Youngeun Kim, Cheol-Hee Kim, NamHee Kim, Byung-Chul Kim, Cecilia Kim, S Kim, Tae-Gyu Kim, Kwan-Suk Kim, Jee Ah Kim, Kyoungtae Kim, Seong Jun Kim, Mi Jeong Kim, Myoung Sook Kim, Chu-Young Kim, Minsu Kim, Seong-Tae Kim, Donghyeon Kim, Sunoh Kim, Yu-Jin Kim, Yul-Ho Kim, Eric Kim, Jae-Young Kim, Jin Hee Kim, Tae Min Kim, Yeji Kim, Yo-Han Kim, Kyong-Tai Kim, Dae-Kyeong Kim, June Hee Kim, Tae Hyun Kim, Leo A Kim, Young S Kim, Min Bum Kim, Min Seo Kim, Seong-Jin Kim, Young-Chul Kim, Jinkyeong Kim, SooHyeon Kim, Kwangwoo Kim, Dong-Hee Kim, Sang Wun Kim, Won J Kim, Seung Won Kim, Ji-Yul Kim, Moo-Yeon Kim, Do Yeon Kim, Jun Seok Kim, Su-Jin Kim, Jewoo Kim, A Ram Kim, Hyung Hoi Kim, Song-Rae Kim, Hye-Ran Kim, Yoongeum Kim, Jeong-Han Kim, Jinsoo Kim, Steve Kim, Taeyoung Kim, Hwi Seung Kim, Hye Ree Kim, Hyeong-Geug Kim, Yu Mi Kim, J H Kim, Suk Jae Kim, Sung-Hee Kim, Na-Young Kim, Minji Kim, Jongkyu Kim, Jae-Yoon Kim, Hyunjin Kim, Helen B Kim, Dong-Yi Kim, Ji-Yun Kim, Sung Woo Kim, Ha-Jung Kim, Yongmin Kim, Han Young Kim, Hyun-Soo Kim, Hyunju Kim, Jin Man Kim, Young Nam Kim, Hye Young Kim, Sung Yeol Kim, Jong-Oh Kim, Y-D Kim, Jong-Hyun Kim, Jenny H Kim, Youngchang Kim, Okhwa Kim, Y A Kim, Won Kyung Kim, Dongjoon Kim, Myung Jin Kim, Hannah Kim, Ick Young Kim, Hyunsoo Kim, Sungjoo Kim, Seonhee Kim, Y-M Kim, Sun Hee Kim, Jung Sun Kim, Ji Young Kim, Sung-Eun Kim, Wun-Jae Kim, Hee Nam Kim, Vladimir Kim, Donghee Kim, Sang Jin Kim, Won Ho Kim, Byeong-Won Kim, Hyung-Goo Kim, J Julie Kim, Jiwon Kim, Eun-Joo Kim, Hyun Soo Kim, Tae-Hyoung Kim, Anna Kim, Gahyun Kim, Jong Hwan Kim, Borahm Kim, Caroline Kim, Andrea J Kim, Yong-Hoon Kim, Jisup Kim, Yong Kyun Kim, Young-Eun Kim, Angela Kim, Tae-Eun Kim, Ji Won Kim, Sang Geon Kim, Young-Cho Kim, Bo Young Kim, Minsoon Kim, Paul Kim, Jeongseon Kim, Tae-Mi Kim, Oc-Hee Kim, Da-Hyun Kim, Jong Geun Kim, Woo Kyung Kim, Jae-Yong Kim, Jaeuk U Kim, Kye Hyun Kim, Dae-Jin Kim, Jun Chul Kim, Dae Keun Kim, You Sun Kim, Heung-Joong Kim, Angela S Kim, Ji-Young Kim, So-Woon Kim, Dayoung Kim, Sangwoo Kim, Eric Eunshik Kim, Yeeun Kim, Jeewoo Kim, Sungmin Kim, Hyun Sil Kim, Young Hee Kim, Kyunga Kim, Donghyun Kim, Sung-Kyu Kim, Hanah Kim, Do-Kyun Kim, Jonggeol Jeffrey Kim, Min Soo Kim, Ju Han Kim, Hyung Yoon Kim, Youngchul Kim, Minhee Kim, Byung-Taek Kim, Sung-Bae Kim, Suk-Jeong Kim, Min-A Kim, Jae T Kim, Dong-Seok Kim, Min-Seon Kim, Hyoun Ju Kim, JungMin Kim, Kwonseop Kim, Kyong Min Kim, Jae-Jung Kim, Howard H Kim, Min-Seo Kim, Minjoo Kim, Sujung Kim, Woo-Kyun Kim, Yongjae Kim, Jong-Kyu Kim, Dong-il Kim, Jeri Kim, Seol-A Kim, Soriul Kim, Kil-Nam Kim, Soo-Rim Kim, Yun-Jin Kim, Yeonjung Kim, Su Jin Kim, Kyung Woo Kim, Yeon-Jung Kim, Jeong Hee Kim, Youn Shic Kim, Dong-Eun Kim, So-Yeon Kim, C H Kim, Sung-Hoon Kim, Namphil Kim, Kyung-Chang Kim, Chan-Hee Kim, Sun Hye Kim, Seulhee Kim, Joonyoung Kim, Gunhee Kim, Joungmok Kim, Seung-Whan Kim, Sang-Woo Kim, Seongmi Kim, Daegyeom Kim, Da Sol Kim, Ellen Kim, Young Rae Kim, Hee-Sun Kim, Seung Jun Kim, Kyungjin Kim, Youn-Kyung Kim, Sunghoon Kim, Jung-Hyun Kim, Young Eun Kim, Ho-Sook Kim, Hyun Ju Kim, Gyeonghun Kim, Baek Kim, Soon-Hee Kim, David E Kim, Joong Sun Kim, Hoon Seok Kim, Yunjung Kim, Keun You Kim, Min Cheol Kim, Gye Lim Kim, Dakyung Kim, Jong Won Kim, Hoon Kim, Seung-Jin Kim, Myeong Ji Kim, NamDoo Kim, Jinho Kim, Hyo Jong Kim, Young-Woong Kim, Un Gi Kim, Tae-Hyun Kim, Kee-Pyo Kim, Oh Yoen Kim, Juyeong Kim, Jun Hee Kim, Chae-Hyun Kim, Leo Kim, Eun Ho Kim, Haeryoung Kim, Seong Kim, Jessica Kim, Jin Won Kim, Hyun Sook Kim, Kyeongmi Kim, Rosalind Kim, Sujin Kim, E Kim, Nam-Hyung Kim, Sin Gon Kim, Seohyun Kim, Boram Kim, Kyeong Jin Kim, Gi Beom Kim, Jason K Kim, Hyung-Seok Kim, Dae Hyun Kim, Jina Kim, Ji-Won Kim, Eui-Soon Kim, Minkyeong Kim, M V Kim, Yumi Kim, Sunyoung Kim, Maya Kim, Mijeong Kim, Hyunbae Kim, Esl Kim, Su Kang Kim, Ju-Ryoung Kim, Bomi Kim, Kyung Han Kim, Seoyoung Kim, Ji-Eun Kim, Yoojin Kim, Minju Kim, Tae-Woon Kim, Jae Gon Kim, Hyeong Su Kim, Choon-Song Kim, Kye Hun Kim, Hyesung Kim, Yeon-Ki Kim, Jaeyoon Kim, Hyeung-Rak Kim, Kook Hwan Kim, Sung Hyun Kim, Sol Kim, Hyunwoo Kim, Min Joo Kim, Dong-Wook Kim, Young Sam Kim, Hye-Yeon Kim, Yun Joong Kim, Ki Woong Kim, Jungsu Kim, Misu Kim, Seung Chul Kim, Mi-Yeon Kim, Hyo-Soo Kim, Won Kon Kim, Sangmi Kim, Jong Deog Kim, Yun Gi Kim, Seon-Young Kim, Il-Sup Kim, Byung Guk Kim, Susy Kim, Youngwoo Kim, Min-Young Kim, Jae-Min Kim, Yong Sung Kim, Young-Won Kim, Jung H Kim, Eun Hee Kim, Yong Kwan Kim, Haelee Kim, Daesik Kim, Gukhan Kim, Hyungjun Kim, Young-Hoon Kim, Jong-Ki Kim, Byron Kim, Taek-Kyun Kim, Bo-Ra Kim, Dokyoon Kim, Min Chul Kim, Miso Kim, Seong-Min Kim, Jang Heub Kim, Hyeyoung Kim, Hyunwook Kim, Hee Su Kim, Young-Joo Kim, Reuben H Kim, Hong-Kook Kim, Soo Jung Kim, Sungryong Kim, Taejung Kim, Jung Soo Kim, Kyoung Hwan Kim, Sung Mok Kim, Daeeun Kim, Hyelim Kim, Beomsoo Kim, Ji-Woon Kim
articles
Seong-Lan Yu, Hyunghee Lee, Jihyun Park +7 more · 2025 · Reproductive medicine and biology · Wiley · added 2026-04-24
Endometrial receptivity is a critical determinant of successful embryo implantation and is intricately linked to the pathophysiology of infertility. This study aimed to elucidate the role of exosomal Show more
Endometrial receptivity is a critical determinant of successful embryo implantation and is intricately linked to the pathophysiology of infertility. This study aimed to elucidate the role of exosomal miR-203a-3p in regulating endometrial receptivity, thereby providing insights into potential therapeutic strategies for infertility treatment. Transcriptomic profiling of exosomes was performed to identify factors associated with endometrial receptivity. miR-203a-3p, exhibiting high expression levels in exosomes, was selected for further investigation. Human endometrial tissues from different menstrual phases and patient groups were analyzed for miR-203a-3p expression. Functional studies using miR-203a-3p mimics and engineered exosomes were conducted in non-receptive AN3-CA cells. During the secretory phase, miR-203a-3p expression was markedly higher in the endometria of fertile women than in those of infertile women. Overexpression of miR-203a-3p, which directly targeted Snail family transcriptional repressor (SNAI1), resulted in increased E-cadherin expression and enhanced spheroid attachment in non-receptive AN3-CA cells. Consistently, delivery of miR-203a-3p mimics via engineered exosomes increased E-cadherin expression by suppressing SNAI1 and enhanced spheroid adhesion in AN3-CA cells. Our data highlight the importance of the miR-203a-3p/SNAI1/E-cadherin axis in governing endometrial receptivity. Exosome-mediated delivery of miR-203a-3p mimics may represent a promising therapeutic strategy for improving embryo implantation and treating infertility. Show less
no PDF DOI: 10.1002/rmb2.12689
SNAI1
Henry D Mauser, Taryn E Keyzer, Jessica M Surma +8 more · 2025 · Virulence · Taylor & Francis · added 2026-04-24
no PDF DOI: 10.1080/21505594.2025.2564281
SNAI1
Hyewon Hur, Hayan Kwon, Yun Ji Jung +7 more · 2025 · Cells · MDPI · added 2026-04-24
During pregnancy, exposure to fine particulate matter (PM
no PDF DOI: 10.3390/cells14171317
SNAI1
Hong-Kook Kim, Heedon Cheong, Moo-Yeon Kim +1 more · 2025 · International journal of nanomedicine · added 2026-04-24
Ovarian cancer is the third most common gynecological cancer worldwide. Due to the high recurrence rate of advanced-stage ovarian cancer, often resulting from drug-resistant and refractory disease, va Show more
Ovarian cancer is the third most common gynecological cancer worldwide. Due to the high recurrence rate of advanced-stage ovarian cancer, often resulting from drug-resistant and refractory disease, various treatment strategies are under investigation. Genome editing of therapeutic target genes holds promise in enhancing cancer treatment efficacy by elucidating gene functions and mechanisms involved in cancer progression. The CRISPR/Cas9 system, in particular, shows great potential in ovarian cancer gene therapy and drug development. Targeting therapeutic genes such as BRCA1/2, P53, Snai1 etc, could improve the therapeutic strategy in ovarian cancer. CRISPR/Cas9 is a powerful gene-editing tool that there are many on-going clinical trials to treat various diseases including cancer. Nano-based delivery systems for CRISPR/Cas9 offer further therapeutic benefits, leveraging the unique properties of nanoparticles to improve delivery efficiency. Nano-based delivery systems could enhance the stability of CRISPR/Cas9 delivery formats (such as plasmid, mRNA, etc) and improve the delivery precision of delivery to target tumors. Additionally, combining CRISPR/Cas9 with targeted drug treatments, especially those aimed at genes associated with drug resistance, may significantly improve therapeutic outcomes in ovarian cancer. In this review, we discuss therapeutic target genes and their mechanisms in ovarian cancer, advances in nano-based CRISPR/Cas9 delivery, and the therapeutic potential of combining CRISPR/Cas9 with drug treatments for ovarian cancer. Show less
no PDF DOI: 10.2147/IJN.S507688
SNAI1
Keun-Seok Hong, Ki-Jun Ryu, Hyemin Kim +8 more · 2025 · Experimental & molecular medicine · Nature · added 2026-04-24
Mitogen- and stress-activated protein kinase 1 (MSK1), a Ser/Thr kinase, phosphorylates nuclear proteins to increase their stability and DNA-binding affinity. Despite the role of MSK1 in promoting can Show more
Mitogen- and stress-activated protein kinase 1 (MSK1), a Ser/Thr kinase, phosphorylates nuclear proteins to increase their stability and DNA-binding affinity. Despite the role of MSK1 in promoting cancer progression in colorectal cancer (CRC), the precise molecular mechanisms remain unelucidated. Here we show that MSK1 expression induces the epithelial-mesenchymal transition (EMT) process and increases CRC cell metastasis. Furthermore, we discovered that MSK1 interacts with Snail, a key EMT regulator, and increases its stability by inhibiting ubiquitin-mediated proteasomal degradation. Importantly, MSK1 increased Snail protein stability by promoting deubiquitination rather than inhibiting its ubiquitination. Finally, we identified USP5 as an essential deubiquitinase that binds to Snail protein phosphorylated by MSK1. Based on the experimental data, in CRC, MSK1-Snail-USP5 axis can promote EMT and metastasis of CRC. Together, our findings provide potential biomarkers and novel therapeutic targets for further research in CRC. Show less
no PDF DOI: 10.1038/s12276-025-01433-0
SNAI1
Kyungwon Kim, Hye Ju Shin, Sang-Cheol Park +7 more · 2025 · Journal of endocrinological investigation · Springer · added 2026-04-24
We aimed to identify differentially expressed spliceosome components in growth hormone (GH)-secreting pituitary tumors and investigate their roles in pathogenesis. We performed transcriptome analysis Show more
We aimed to identify differentially expressed spliceosome components in growth hormone (GH)-secreting pituitary tumors and investigate their roles in pathogenesis. We performed transcriptome analysis of 20 somatotroph adenomas and 6 normal pituitary tissues to select dysregulated spliceosome components. Clinical characteristics were analyzed based on gene expression in 64 patients with acromegaly. Proliferation, invasion, and hormonal activity of GH secreting pituitary adenoma cells were investigated. TCERG1 expression was significantly higher in somatotroph adenomas than in normal pituitaries (log2 fold change 0.59, adjusted P = 0.0002 Spliceosome machinery provide novel insights into the pathogenesis of GH-secreting pituitary tumor and highlight the potential role of TCERG1 as a biomarker for tumor aggressiveness. Show less
no PDF DOI: 10.1007/s40618-024-02447-7
SNAI1
Wilfredo G Gonzalez Rivera, Youwen Liu, Tara Mirmira +6 more · 2025 · medRxiv : the preprint server for health sciences · added 2026-04-24
Genetic studies have largely focused on homogeneous populations, limiting our understanding of the genetic architecture of complex traits in admixed individuals. The advent of diverse biobanks like th Show more
Genetic studies have largely focused on homogeneous populations, limiting our understanding of the genetic architecture of complex traits in admixed individuals. The advent of diverse biobanks like the Show less
no PDF DOI: 10.64898/2025.12.29.25343152
ZPR1
Jiwon Ko, Soyoung Jang, Soyeon Jang +7 more · 2024 · BMB reports · added 2026-04-24
Glucose-dependent insulinotropic polypeptide (GIP), a 42-aminoacid hormone, exerts multifaceted effects in physiology, most notably in metabolism, obesity, and inflammation. Its significance extends t Show more
Glucose-dependent insulinotropic polypeptide (GIP), a 42-aminoacid hormone, exerts multifaceted effects in physiology, most notably in metabolism, obesity, and inflammation. Its significance extends to neuroprotection, promoting neuronal proliferation, maintaining physiological homeostasis, and inhibiting cell death, all of which play a crucial role in the context of neurodegenerative diseases. Through intricate signaling pathways involving its cognate receptor (GIPR), a member of the G protein-coupled receptors, GIP maintains cellular homeostasis and regulates a defense system against ferroptosis, an essential process in aging. Our study, utilizing GIP-overexpressing mice and in vitro cell model, elucidates the pivotal role of GIP in preserving neuronal integrity and combating age-related damage, primarily through the Epac/Rap1 pathway. These findings shed light on the potential of GIP as a therapeutic target for the pathogenesis of ferroptosis in neurodegenerative diseases and aging. [BMB Reports 2024; 57(9): 417-423]. Show less
📄 PDF DOI: 10.5483/BMBRep.2024-0067
GIPR
Sun Hee Kim, Sangdon Han, Jian Zhao +10 more · 2024 · ACS medicinal chemistry letters · ACS Publications · added 2026-04-24
A novel class of nonpeptide melanocortin type 2 receptor (MC2R) antagonists was discovered through modification of known nonpeptide MC4R ligands. Structure-activity relationship (SAR) studies led to t Show more
A novel class of nonpeptide melanocortin type 2 receptor (MC2R) antagonists was discovered through modification of known nonpeptide MC4R ligands. Structure-activity relationship (SAR) studies led to the discovery of Show less
no PDF DOI: 10.1021/acsmedchemlett.3c00514
MC4R
Connor Laule, Nilufer Sayar-Atasoy, Iltan Aklan +4 more · 2024 · Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · Nature · added 2026-04-24
Stress is thought to be an important contributing factor for eating disorders; however, neural substrates underlying the complex relationship between stress and appetite are not fully understood. Usin Show more
Stress is thought to be an important contributing factor for eating disorders; however, neural substrates underlying the complex relationship between stress and appetite are not fully understood. Using in vivo recordings from awake behaving mice, we show that various acute stressors activate catecholaminergic nucleus tractus solitarius (NTS Show less
no PDF DOI: 10.1038/s41386-024-01810-9
MC4R
Jonggeol Jeffrey Kim, Sara Bandres-Ciga, Karl Heilbron +3 more · 2024 · NPJ Parkinson's disease · Nature · added 2026-04-24
Hyposmia (decreased smell function) is a common early symptom of Parkinson's disease (PD). The shared genetic architecture between hyposmia and PD is unknown. We leveraged genome-wide association stud Show more
Hyposmia (decreased smell function) is a common early symptom of Parkinson's disease (PD). The shared genetic architecture between hyposmia and PD is unknown. We leveraged genome-wide association study (GWAS) results for self-assessment of 'ability to smell' and PD diagnosis to determine shared genetic architecture between the two traits. Linkage disequilibrium score (LDSC) regression found that the sense of smell negatively correlated at a genome-wide level with PD. Local Analysis of [co]Variant Association (LAVA) found negative correlations in four genetic loci near GBA1, ANAPC4, SNCA, and MAPT, indicating shared genetic liability only within a subset of prominent PD risk genes. Using Mendelian randomization, we found evidence for a strong causal relationship between PD and liability towards poorer sense of smell, but weaker evidence for the reverse direction. This work highlights the heritability of olfactory function and its relationship with PD heritability and provides further insight into the association between PD and hyposmia. Show less
📄 PDF DOI: 10.1038/s41531-024-00838-4
ANAPC4
Le Phuong Nguyen, Wenxin Song, Ye Yang +21 more · 2024 · JCI insight · added 2026-04-24
Lipoprotein lipase (LPL) and multiple regulators of LPL activity (e.g., APOC2 and ANGPTL4) are present in all vertebrates, but GPIHBP1-the endothelial cell (EC) protein that captures LPL within the su Show more
Lipoprotein lipase (LPL) and multiple regulators of LPL activity (e.g., APOC2 and ANGPTL4) are present in all vertebrates, but GPIHBP1-the endothelial cell (EC) protein that captures LPL within the subendothelial spaces and transports it to its site of action in the capillary lumen-is present in mammals but in not chickens or other lower vertebrates. In mammals, GPIHBP1 deficiency causes severe hypertriglyceridemia, but chickens maintain low triglyceride levels despite the absence of GPIHBP1. To understand intravascular lipolysis in lower vertebrates, we examined LPL expression in mouse and chicken hearts. In both species, LPL was abundant on capillaries, but the distribution of Lpl transcripts was strikingly different. In mouse hearts, Lpl transcripts were extremely abundant in cardiomyocytes but were barely detectable in capillary ECs. In chicken hearts, Lpl transcripts were absent in cardiomyocytes but abundant in capillary ECs. In zebrafish hearts, lpl transcripts were also in capillary ECs but not cardiomyocytes. In both mouse and chicken hearts, LPL was present, as judged by immunogold electron microscopy, in the glycocalyx of capillary ECs. Thus, mammals produce LPL in cardiomyocytes and rely on GPIHBP1 to transport the LPL into capillaries, whereas lower vertebrates produce LPL directly in capillary ECs, rendering an LPL transporter unnecessary. Show less
📄 PDF DOI: 10.1172/jci.insight.184940
ANGPTL4
Min Seok Park, Sang Eun Kim, Pureunchowon Lee +3 more · 2024 · BMB reports · added 2026-04-24
Angiopoietin-like 4 (ANGPTL4) has been identified as an adipokine involved in several non-metabolic and metabolic diseases, including angiogenesis, glucose homeostasis, and lipid metabolism. To date, Show more
Angiopoietin-like 4 (ANGPTL4) has been identified as an adipokine involved in several non-metabolic and metabolic diseases, including angiogenesis, glucose homeostasis, and lipid metabolism. To date, the role of ANGPTL4 in cancer growth and progression, and metastasis, has been variable. Accumulating evidence suggests that proteolytic processing and posttranslational modifications of ANGPTL4 can significantly alter its function, and may contribute to the multiple and conflicting roles of ANGPTL4 in a tissue-dependent manner. With the growing interest in ANGPTL4 in cancer diagnosis and therapy, we aim to provide an up-to-date review of the implications of ANGPTL4 as a biomarker/oncogene in cancer metabolism, metastasis, and the tumor microenvironment (TME). In cancer cells, ANGPTL4 plays an important role in regulating metabolism by altering intracellular glucose, lipid, and amino acid metabolism. We also highlight the knowledge gaps and future prospect of ANGPTL4 in lymphatic metastasis and perineural invasion through various signaling pathways, underscoring its importance in cancer progression and prognosis. Through this review, a better understanding of the role of ANGPTL4 in cancer progression within the TME will provide new insights into other aspects of tumorigenesis and the potential therapeutic value of ANGPTL4. [BMB Reports 2024; 57(8): 343-351]. Show less
📄 PDF DOI: 10.5483/BMBRep.2024-0082
ANGPTL4
Seyedeh Fatemeh Razavipour, Hyunho Yoon, Kibeom Jang +13 more · 2024 · Nature communications · Nature · added 2026-04-24
In many cancers, a stem-like cell subpopulation mediates tumor initiation, dissemination and drug resistance. Here, we report that cancer stem cell (CSC) abundance is transcriptionally regulated by C- Show more
In many cancers, a stem-like cell subpopulation mediates tumor initiation, dissemination and drug resistance. Here, we report that cancer stem cell (CSC) abundance is transcriptionally regulated by C-terminally phosphorylated p27 (p27pT157pT198). Mechanistically, this arises through p27 co-recruitment with STAT3/CBP to gene regulators of CSC self-renewal including MYC, the Notch ligand JAG1, and ANGPTL4. p27pTpT/STAT3 also recruits a SIN3A/HDAC1 complex to co-repress the Pyk2 inhibitor, PTPN12. Pyk2, in turn, activates STAT3, creating a feed-forward loop increasing stem-like properties in vitro and tumor-initiating stem cells in vivo. The p27-activated gene profile is over-represented in STAT3 activated human breast cancers. Furthermore, mammary transgenic expression of phosphomimetic, cyclin-CDK-binding defective p27 (p27CK-DD) increases mammary duct branching morphogenesis, yielding hyperplasia and microinvasive cancers that can metastasize to liver, further supporting a role for p27pTpT in CSC expansion. Thus, p27pTpT interacts with STAT3, driving transcriptional programs governing stem cell expansion or maintenance in normal and cancer tissues. Show less
📄 PDF DOI: 10.1038/s41467-024-48742-y
ANGPTL4
Se-Ra Park, Eun-Kyung Min, Soo-Rim Kim +6 more · 2024 · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · Wiley · added 2026-04-24
Adapted immune cells are known to develop memory functions that increase resistance to subsequent infections after initial pathogen exposure, however, it is unclear whether non-immune cells, like tiss Show more
Adapted immune cells are known to develop memory functions that increase resistance to subsequent infections after initial pathogen exposure, however, it is unclear whether non-immune cells, like tissue-resident stem cells, have similar memory functions. Here, it is found that tissue-resident stem cells crucial for tissue regeneration show diminished adverse effects on diverse stem cell functions against successive exposure to foreign antigen (β-glucan) to maintain tissue homeostasis and stability both in vitro and in vivo. These data suggest that endometrial stem cells may possess a robust memory function, in contrast, fully differentiated cells like fibroblasts and vesicular cells do not show these memory mechanisms upon consecutive antigen exposure. Moreover, the pivotal role of Angiopoietin-like 4 (ANGPTL4) in regulating the memory functions of endometrial stem cells is identified through specific shRNA knockdown in vitro and knockout mice in vivo experiments. ANGPTL4 is associated with the alteration of diverse stem cell functions and epigenetic modifications, notably through histone H3 methylation changes and two pathways (i.e., PI3K/Akt and FAK/ERK1/2 signaling) upon consecutive antigen exposure. These findings imply the existence of inherent self-defense mechanisms through which local stem cells can adapt and protect themselves from recurrent antigenic challenges, ultimately mitigating adverse consequences. Show less
📄 PDF DOI: 10.1002/advs.202307545
ANGPTL4
Eun-Kyung Min, Soo-Rim Kim, Choon-Mi Lee +5 more · 2024 · Molecular therapy : the journal of the American Society of Gene Therapy · Elsevier · added 2026-04-24
Although memory functions of immune cells characterized by increased resistance to subsequent infections after initial pathogen exposure are well-established, it remains unclear whether non-immune cel Show more
Although memory functions of immune cells characterized by increased resistance to subsequent infections after initial pathogen exposure are well-established, it remains unclear whether non-immune cells, especially tissue-resident stem cells, exhibit similar memory mechanisms. The present study revealed that detrimental effects of initial viral antigen exposure (human papillomavirus [HPV]) on diverse stem cell functions were significantly exacerbated upon subsequent secondary exposure both in vitro and in vivo. Importantly, endometrial stem cells exhibited robust memory functions following consecutive HPV antigen exposures, whereas fully differentiated cells such as fibroblasts and vesicular cells did not show corresponding changes in response to the same antigen exposures. Deficiency of angiopoietin-like 4 (ANGPTL4) achieved through small hairpin RNA knockdown in vitro and knockout (KO) mice in vivo highlighted the critical role of ANGPTL4 in governing memory functions associated with various stem cell processes. This regulation occurred through histone H3 methylation alterations and PI3K/Akt signaling pathways in response to successive HPV antigen exposures. Furthermore, memory functions associated with various stem cell functions that were evident in wild-type mice following consecutive exposures to HPV antigen were not observed in ANGPTL4 KO mice. In summary, our findings strongly support the presence of memory mechanism in non-immune cells, particularly tissue-resident stem cells. Show less
no PDF DOI: 10.1016/j.ymthe.2024.04.006
ANGPTL4
Hiroshi Kumagai, Su-Jeong Kim, Brendan Miller +9 more · 2024 · American journal of physiology. Endocrinology and metabolism · added 2026-04-24
Mitochondrial open reading frame of the 12S ribosomal RNA type-c (MOTS-c), a mitochondrial microprotein, has been described as a novel regulator of glucose and lipid metabolism. In addition to its rol Show more
Mitochondrial open reading frame of the 12S ribosomal RNA type-c (MOTS-c), a mitochondrial microprotein, has been described as a novel regulator of glucose and lipid metabolism. In addition to its role as a metabolic regulator, MOTS-c prevents skeletal muscle atrophy in high fat-fed mice. Here, we examined the preventive effect of MOTS-c on skeletal muscle mass, using an immobilization-induced muscle atrophy model, and explored its underlying mechanisms. Male C57BL/6J mice (10 wk old) were randomly assigned to one of the three experimental groups: nonimmobilization control group (sterilized water injection), immobilization control group (sterilized water injection), and immobilization and MOTS-c-treated group (15 mg/kg/day MOTS-c injection). We used casting tape for the immobilization experiment. After 8 days of the experimental period, skeletal muscle samples were collected and used for Western blotting, RNA sequencing, and lipid and collagen assays. Immobilization reduced ∼15% of muscle mass, whereas MOTS-c treatment attenuated muscle loss, with only a 5% reduction. MOTS-c treatment also normalized phospho-AKT, phospho-FOXO1, and phospho-FOXO3a expression levels and reduced circulating inflammatory cytokines, such as interleukin-1b (IL-1β), interleukin-6 (IL-6), chemokine C-X-C motif ligand 1 (CXCL1), and monocyte chemoattractant protein 1 (MCP-1), in immobilized mice. Unbiased RNA sequencing and its downstream analyses demonstrated that MOTS-c modified adipogenesis-modulating gene expression within the peroxisome proliferator-activated receptor (PPAR) pathway. Supporting this observation, muscle fatty acid levels were lower in the MOTS-c-treated group than in the casted control mice. These results suggest that MOTS-c treatment inhibits skeletal muscle lipid infiltration by regulating adipogenesis-related genes and prevents immobilization-induced muscle atrophy. Show less
no PDF DOI: 10.1152/ajpendo.00285.2023
ANGPTL4
Mingyu Lee, Yong Sook Kim, Junggeon Park +8 more · 2024 · Bioactive materials · Elsevier · added 2026-04-24
The infarcted heart undergoes irreversible pathological remodeling after reperfusion involving left ventricle dilation and excessive inflammatory reactions in the infarcted heart, frequently leading t Show more
The infarcted heart undergoes irreversible pathological remodeling after reperfusion involving left ventricle dilation and excessive inflammatory reactions in the infarcted heart, frequently leading to fatal functional damage. Extensive attempts have been made to attenuate pathological remodeling in infarcted hearts using cardiac patches and anti-inflammatory drug delivery. In this study, we developed a paintable and adhesive hydrogel patch using dextran-aldehyde (dex-ald) and gelatin, incorporating the anti-inflammatory protein, ANGPTL4, into the hydrogel for sustained release directly to the infarcted heart to alleviate inflammation. We optimized the material composition, including polymer concentration and molecular weight, to achieve a paintable, adhesive hydrogel using 10% gelatin and 5% dex-ald, which displayed in-situ gel formation within 135 s, cardiac tissue-like modulus (40.5 kPa), suitable tissue adhesiveness (4.3 kPa), and excellent mechanical stability. ANGPTL4 was continuously released from the gelatin/dex-ald hydrogel without substantial burst release. The gelatin/dex-ald hydrogel could be conveniently painted onto the beating heart and degraded in vivo. Moreover, in vivo studies using animal models of acute myocardial infarction revealed that our hydrogel cardiac patch containing ANGPTL4 significantly improved heart tissue repair, evaluated by echocardiography and histological evaluation. The heart tissues treated with ANGPTL4-loaded hydrogel patches exhibited increased vascularization, reduced inflammatory macrophages, and structural maturation of cardiac cells. Our novel hydrogel system, which allows for facile paintability, appropriate tissue adhesiveness, and sustained release of anti-inflammatory drugs, will serve as an effective platform for the repair of various tissues, including heart, muscle, and cartilage. Show less
📄 PDF DOI: 10.1016/j.bioactmat.2023.08.020
ANGPTL4
Young Jun Park, Sungji Moon, Jaeyong Choi +5 more · 2024 · Lipids in health and disease · BioMed Central · added 2026-04-24
Genome-wide association studies (GWAS) of metabolic syndrome (MetS) have predominantly focused on non-Asian populations, with limited representation from East Asian cohorts. Moreover, previous GWAS an Show more
Genome-wide association studies (GWAS) of metabolic syndrome (MetS) have predominantly focused on non-Asian populations, with limited representation from East Asian cohorts. Moreover, previous GWAS analyses have primarily emphasized the significance of top single nucleotide polymorphisms (SNPs), poorly explaining other SNP signals in linkage disequilibrium. This study aimed to reveal the interaction between rs651821 and rs2266788, the principal variants of apolipoprotein A5 (APOA5), within the most significant loci identified through GWAS on MetS. GWAS on MetS and its components was conducted using the data from the Korean Genome and Epidemiology Study (KoGES) city cohort comprising 58,600 individuals with available biochemical, demographic, lifestyle factors, and the most significant APOA5 locus was analyzed further in depth. According to GWAS of MetS and its diagnostic components, a significant association between the APOA5 SNPs rs651821/rs2266788 and MetS/triglycerides/high-density lipoprotein phenotypes was revealed. However, a conditional analysis employing rs651821 unveiled a reversal in the odds ratio for rs2266788. Therefore, rs651821 and rs2266788 emerged as independent and opposing signals in the extended GWAS analysis, i.e., the multilayered effects. Further gene-environment interaction analyses regarding lifestyle factors such as smoking, alcohol consumption, and physical activity underscored these multilayered effects. This study unveils the intricate interplay between rs651821 and rs2266788 derived from MetS GWAS. Removing the influence of lead SNP reveals an independent protective signal associated with rs2266788, suggesting a multilayered effect between these SNPs. These findings underline the need for novel perspectives in future MetS GWAS. Show less
📄 PDF DOI: 10.1186/s12944-024-02248-0
APOA5
Jimi Kim, Younghwa Baek, Siwoo Lee · 2024 · Nutrition & metabolism · BioMed Central · added 2026-04-24
Consumption of dietary fiber has been suggested as an important aspect of a healthy diet to reduce the risk of metabolic syndrome (MetS), including cardiovascular disease. The role of fiber intake in Show more
Consumption of dietary fiber has been suggested as an important aspect of a healthy diet to reduce the risk of metabolic syndrome (MetS), including cardiovascular disease. The role of fiber intake in MetS might differ by individual genetic susceptibility. APOA5 encodes a regulator of plasma triglyceride levels, which impacts the related mechanisms of MetS. This study investigated the association between dietary fiber and the risk of MetS, assessing their associations according to APOA5 genetic variants. A total of 1985 participants aged 30-55 years were included from a cross-sectional study based on the Korean Medicine Daejeon Citizen Cohort study at baseline (2017-2019). Dietary fiber intake was measured using a semiquantitative food frequency questionnaire. The APOA5 polymorphisms (rs2266788 A > G, rs662799 A > G, and rs651821 T > C) were genotyped using the Asia Precision Medicine Research Array. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs). A higher consumption of dietary fiber was associated with a lower prevalence of MetS (P = 0.025). Among the components of MetS, an inverse association with dietary fiber was observed in increased waist circumference (OR, 95% CI = 0.60, 0.41-0.88, P for trend = 0.009) and elevated triglycerides (OR, 95% CI = 0.69, 0.50-0.96, P for trend = 0.012). Regarding the interaction with APOA5 genetic variants, a stronger association with dietary fiber intake was shown in G allele carriers of rs662799 than in A/A carriers (OR, 95% CI = 2.34, 1.59-3.44, P for interaction = 0.024) and in C allele carriers of rs651821 than in T/T carriers (OR, 95% CI = 2.35, 1.59-3.46, P for interaction = 0.027). The findings of this study suggest that the benefits of dietary fiber on the risk of MetS could be modified by genetic variants of the APOA5 gene, providing a more effective strategy for preventing MetS. Show less
📄 PDF DOI: 10.1186/s12986-024-00793-0
APOA5
Ngoc-Thanh Kim, Doan-Loi Do, Mai-Ngoc Thi Nguyen +3 more · 2024 · Bioinformatics and biology insights · SAGE Publications · added 2026-04-24
Atherosclerotic cardiovascular diseases (CVDs) are closely linked to factors such as familial hypercholesterolemia (FH), often caused by mutations in low-density lipoprotein receptor (
📄 PDF DOI: 10.1177/11779322241301267
APOB
Seohyun Kim, Chin Kook Rhee, Yong Suk Jo +4 more · 2024 · Scientific reports · Nature · added 2026-04-24
Previous studies suggest associations between the risk of developing chronic obstructive pulmonary disease (COPD) and adiponectin/leptin (ALR) and apolipoprotein B/A1 (APOR) ratios. This longitudinal Show more
Previous studies suggest associations between the risk of developing chronic obstructive pulmonary disease (COPD) and adiponectin/leptin (ALR) and apolipoprotein B/A1 (APOR) ratios. This longitudinal observational study, using data from the Korean Genome and Epidemiology Study (KoGES), examined the rate of lung function decline, risk factors for the airflow obstruction (AFO), and the time to first AFO based on ALR and APOR groups. Among 5578 participants, high ALR and low APOR were associated with rapid decline in lung function and a shorter time to the first AFO. The high ALR group and the combined high ALR and low APOR group showed higher risk of experiencing AFO both at least once (RR 1.46, 95% CI 1.12-1.90; RR 1.74, 95% CI 1.23-2.46, respectively) and at the final follow up (RR 1.44, 95% CI 1.05-1.96; RR 1.72, 95% CI 1.14-2.60, respectively). High ALR and the combined high ALR and low APOR were identified as risk factors for earlier time to first AFO. This study highlights the potential of ALR and APOR as makers for predicting the risk of future airflow obstruction. Show less
📄 PDF DOI: 10.1038/s41598-024-80055-4
APOB
Hong-Gi Kim, Jin-Ho Park, Ha-Hyun Shin +7 more · 2024 · Scientific reports · Nature · added 2026-04-24
Metabolic dysfunction-associated fatty liver disease (MAFLD) is a common liver disease associated with obesity and is caused by the accumulation of ectopic fat without alcohol consumption. Coxsackievi Show more
Metabolic dysfunction-associated fatty liver disease (MAFLD) is a common liver disease associated with obesity and is caused by the accumulation of ectopic fat without alcohol consumption. Coxsackievirus and adenovirus receptor (CAR) are vital for cardiac myocyte-intercalated discs and endothelial cell-to-cell tight junctions. CAR has also been reported to be associated with obesity and high blood pressure. However, its function in the liver is still not well understood. The liver of obese mice exhibit elevated CAR mRNA and protein levels. Furthermore, in the liver of patients with non-alcoholic steatohepatitis, CAR is reduced in hepatocyte cell-cell junctions compared to normal levels. We generated liver-specific CAR knockout (KO) mice to investigate the role of CAR in the liver. Body and liver weights were not different between wild-type (WT) and KO mice fed a paired or high-fat diet (HFD). However, HFD induced significant liver damage and lipid accumulation in CAR KO mice compared with WT mice. Additionally, inflammatory cytokines transcription, hepatic permeability, and macrophage recruitment considerably increased in CAR KO mice. We identified a new interaction partner of CAR using a protein pull-down assay and mass spectrometry. Apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3C (APOBEC3C) demonstrated a complex relationship with CAR, and hepatic CAR expression tightly regulated its level. Moreover, Apolipoprotein B (ApoB) and Low-density lipoprotein receptor (LDLR) levels correlated with APOBEC3C expression in the liver of CAR KO mice, suggesting that CAR may regulate lipid accumulation by controlling APOBEC3C activity. In this study, we showed that hepatic CAR deficiency increased cell-to-cell permeability. In addition, CAR deletion significantly increased hepatic lipid accumulation by inducing ApoB and LDLR expression. Although the underlying mechanism is unclear, CARs may be a target for the development of novel therapies for MAFLD. Show less
📄 PDF DOI: 10.1038/s41598-024-72561-2
APOB
Soo-Yeon Park, Tae Gwon Park, Kwanyong Choi +2 more · 2024 · Nutrients · MDPI · added 2026-04-24
📄 PDF DOI: 10.3390/nu16172864
APOB
Jung-Ho Yang, Kyung Hoon Cho, Young Joon Hong +3 more · 2024 · Korean circulation journal · added 2026-04-24
Familial hypercholesterolemia (FH) increases the risk of premature cardiovascular disease through disrupted low-density lipoprotein cholesterol (LDL-C) metabolism. Although FH is a severe condition, i Show more
Familial hypercholesterolemia (FH) increases the risk of premature cardiovascular disease through disrupted low-density lipoprotein cholesterol (LDL-C) metabolism. Although FH is a severe condition, it remains widely underdiagnosed, which can be attributed to barriers in genetic testing and a lack of awareness. This study aims to propose and evaluate a targeted screening program for FH in South Korea by integrating the General Health Screening Program (GHSP) with cascade genetic screening. The study included individuals with LDL-C levels ≥190 mg/dL identified during the 2021 GHSP (primary participants). Data on demographics, lifestyle, medical history, and family history were collected through questionnaires. Targeted next-generation sequencing was used to identify pathogenic mutations in the Among 83 individuals with severe hypercholesterolemia identified through the GHSP, 7 primary participants (8.4%) carried pathogenic mutations in the Integrating community resources with FH screening can enhance the early detection and treatment of FH. By utilizing GHSP data and adding genetic screening, the proposed model provides a strategy to reduce the cardiovascular risks associated with FH, supporting its wider adoption at the national level. Show less
📄 PDF DOI: 10.4070/kcj.2024.0107
APOB
Hwi Seung Kim, Yun Kyung Cho, Myung Jin Kim +5 more · 2024 · Frontiers in endocrinology · Frontiers · added 2026-04-24
Myosteatosis, ectopic fat accumulation in skeletal muscle, is a crucial component of sarcopenia, linked to various cardiometabolic diseases. This study aimed to analyze the association between dyslipi Show more
Myosteatosis, ectopic fat accumulation in skeletal muscle, is a crucial component of sarcopenia, linked to various cardiometabolic diseases. This study aimed to analyze the association between dyslipidemia and myosteatosis using abdominal computed tomography (CT) in a large population. This study included 11,823 patients not taking lipid-lowering medications with abdominal CT taken between 2012 and 2013. Total abdominal muscle area (TAMA), measured at the L3 level, was segmented into skeletal muscle area (SMA) and intramuscular adipose tissue. SMA was further classified into normal attenuation muscle area (NAMA: good quality muscle) and low attenuation muscle area (poor quality muscle). NAMA divided by TAMA (NAMA/TAMA) represents good quality muscle. Atherosclerotic dyslipidemia was defined as high-density lipoprotein cholesterol (HDL-C) less than 40 mg/dL in men and 50 mg/dL in women, low-density lipoprotein cholesterol (LDL-C) greater than 160 mg/dL, triglycerides (TG) greater than 150 mg/dL, small dense LDL-C (sdLDL-C) greater than 50.0 mg/dL, or apolipoprotein B/A1 (apoB/A1) greater than 0.08. The adjusted odds ratios (ORs) of dyslipidemia according to the HDL-C and sdLDL definitions were greater in both sexes in the lower quartiles (Q1~3) of NAMA/TAMA compared with Q4. As per other definitions, the ORs were significantly increased in only women for LDL-C and only men for TG and ApoB/A1. In men, all lipid parameters were significantly associated with NAMA/TAMA, while TG and ApoB/A1 did not show significant association in women. Myosteatosis measured in abdominal CT was significantly associated with a higher risk of dyslipidemia. Myosteatosis may be an important risk factor for dyslipidemia and ensuing cardiometabolic diseases. Show less
📄 PDF DOI: 10.3389/fendo.2024.1327522
APOB
Nguyen Tran Nam Tien, Trinh Tam Anh, Nguyen Thi Hai Yen +6 more · 2024 · Toxicology mechanisms and methods · Taylor & Francis · added 2026-04-24
Cyclosporine A (CsA) has shown efficacy against immunity-related diseases despite its toxicity in various organs, including the liver, emphasizing the need to elucidate its underlying hepatotoxicity m Show more
Cyclosporine A (CsA) has shown efficacy against immunity-related diseases despite its toxicity in various organs, including the liver, emphasizing the need to elucidate its underlying hepatotoxicity mechanism. This study aimed to capture the alterations in genome-wide expression over time and the subsequent perturbations of corresponding pathways across species. Six data from humans, mice, and rats, including animal liver tissue, human liver microtissues, and two liver cell lines exposed to CsA toxic dose, were used. The microtissue exposed to CsA for 10 d was analyzed to obtain dynamically differentially expressed genes (DEGs). Single-time points data at 1, 3, 5, 7, and 28 d of different species were used to provide additional evidence. Using liver microtissue-based longitudinal design, DEGs that were consistently up- or down-regulated over time were captured, and the well-known mechanism involved in CsA toxicity was elucidated. Thirty DEGs that consistently changed in longitudinal data were also altered in 28-d rat in-house data with concordant expression. Some genes (e.g. Show less
no PDF DOI: 10.1080/15376516.2024.2371894
APOB
Dae Hyun Kim, Seulah Lee, Sang Gyun Noh +2 more · 2024 · Aging · Impact Journals · added 2026-04-24
FoxO6, an identified factor, induces hyperlipidemia and hepatic steatosis during aging by activating hepatic lipoprotein secretion and lipogenesis leading to increased ApoC3 concentrations in the bloo Show more
FoxO6, an identified factor, induces hyperlipidemia and hepatic steatosis during aging by activating hepatic lipoprotein secretion and lipogenesis leading to increased ApoC3 concentrations in the bloodstream. However, the intricate mechanisms underlying hepatic steatosis induced by elevated FoxO6 under hyperglycemic conditions remain intricate and require further elucidation. In order to delineate the regulatory pathway involving ApoC3 controlled by FoxO6 and its resultant functional impacts, we employed a spectrum of models including liver cell cultures, aged rats subjected to HFD, transgenic mice overexpressing FoxO6 (FoxO6-Tg), and FoxO6 knockout mice (FoxO6-KO). Our findings indicate that FoxO6 triggered ApoC3-driven lipid accumulation in the livers of aged rats on an HFD and in FoxO6-Tg, consequently leading to hepatic steatosis and hyperglycemia. Conversely, the absence of FoxO6 attenuated the expression of genes involved in lipogenesis, resulting in diminished hepatic lipid accumulation and mitigated hyperlipidemia in murine models. Additionally, the upregulation of FoxO6 due to elevated glucose levels led to increased ApoC3 expression, consequently instigating cellular triglyceride mediated lipid accumulation. The transcriptional activation of FoxO6 induced by both the HFD and high glucose levels resulted in hepatic steatosis by upregulating ApoC3 and genes associated with gluconeogenesis in aged rats and liver cell cultures. Our conclusions indicate that the upregulation of ApoC3 by FoxO6 promotes the development of hyperlipidemia, hyperglycemia, and hepatic steatosis Show less
📄 PDF DOI: 10.18632/aging.205610
APOC3
Kyung Jae Lee, Jin Soo Moon, Jin Gyu Lim +5 more · 2024 · Journal of gastroenterology and hepatology · Blackwell Publishing · added 2026-04-24
The aim of this study was to investigate the comprehensive genetic effects of exploratory variants of LYPLAL1, GCKR, HSD17B13, TRIB1, APOC3, MBOAT7, and PARVB on pediatric nonalcoholic fatty liver dis Show more
The aim of this study was to investigate the comprehensive genetic effects of exploratory variants of LYPLAL1, GCKR, HSD17B13, TRIB1, APOC3, MBOAT7, and PARVB on pediatric nonalcoholic fatty liver disease in addition to the previously reported variants of TM6SF2, PNPLA3, and SAMM50 in Korean children. A prospective case-control study was conducted involving 309 patients diagnosed using ultrasound and 339 controls. Anthropometric measurements, liver function tests, and metabolic marker analysis were conducted, and fibrosis scores were calculated. Transient elastography was performed in 69 some patients with nonalcoholic fatty liver disease. TaqMan allelic discrimination assays were used for genotyping. The genetic risk scores were calculated using significant variants, namely, HSD17B13, PARVB, PNPLA3, SAMM50, and TM6SF2, to evaluate the additive effect. Risk allele carriers of the PARVB variant showed significantly higher levels of aminotransferases, gamma-glutamyl transferase, alkaline phosphatase, pediatric nonalcoholic fatty liver disease fibrosis score, and aspartate aminotransferase/platelet ratio index. Individuals with a homozygous variant of HSD17B13 showed significantly lower levels of aminotransferase, gamma-glutamyl transferase, liver stiffness measurement, and aspartate aminotransferase/platelet ratio index than those with other genotypes. These parameters did not significantly differ among other variants of LYPLAL1, GCKR, TRIB1, APOC3, and MBOAT7. The genetic risk scores was identified as an independent risk factor for nonalcoholic fatty liver disease and had a positive association with severity. HSD17B13 has protective effects on the severity of pediatric nonalcoholic fatty liver disease. Variants of HSD17B13, PARVB, PNPLA3, SAMM50, and TM6SF2 had an additive effect on nonalcoholic fatty liver disease. Show less
no PDF DOI: 10.1111/jgh.16521
APOC3
Yoon-Seo Choi, Jin-Gwen Hong, Dong-Young Lim +5 more · 2024 · Current issues in molecular biology · MDPI · added 2026-04-24
Melanocytes, located in the epidermis' basal layer, are responsible for melanin pigment production, crucial for skin coloration and protection against UV radiation-induced damage. Melanin synthesis is Show more
Melanocytes, located in the epidermis' basal layer, are responsible for melanin pigment production, crucial for skin coloration and protection against UV radiation-induced damage. Melanin synthesis is intricately regulated by various factors, including the Wnt signaling pathway, particularly mediated by the microphthalmia-associated transcription factor (MITF). While MITF is recognized as a key regulator of pigmentation, its regulation by the Wnt pathway remains poorly understood. This study investigates the role of Sfrp5pepD, a peptide antagonist of the Wnt signaling pathway, in modulating melanogenesis and its potential therapeutic implications for pigmentary disorders. To tackle this issue, we investigated smaller peptides frequently utilized in cosmetics or pharmaceuticals. Nevertheless, there is a significant scarcity of reports on peptides associated with melanin-related signal modulation or inhibiting melanin production. Results indicate that Sfrp5pepD effectively inhibits Wnt signaling by disrupting the interaction between Axin-1 and β-catenin, thus impeding downstream melanogenic processes. Additionally, Sfrp5pepD suppresses the interaction between MITF and β-catenin, inhibiting their nuclear translocation and downregulating melanogenic enzyme expression, ultimately reducing melanin production. These inhibitory effects are validated in cell culture models suggesting potential clinical applications for hyperpigmentation disorders. Overall, this study elucidates the intricate interplay between Wnt signaling and melanogenesis, highlighting Sfrp5pepD as a promising therapeutic agent for pigmentary disorders. Sfrp5pepD, with a molecular weight of less than 500 Da, is anticipated to penetrate the skin unlike SFRPs. This suggests a strong potential for their use as cosmetics or transdermal absorption agents. Additional investigation into its mechanisms and clinical significance is necessary to enhance its effectiveness in addressing melanin-related skin conditions. Show less
📄 PDF DOI: 10.3390/cimb46060324
AXIN1