👤 Lale Tokgözoğlu

Elite training induces profound physiological adaptations, yet whether these changes manifest as stable circulating proteomes remains unclear. This study characterized serum proteomic profiles in male and female Olympic-level athletes to identify biomarkers associated with long-term endurance and strength training. Cross-sectional study in Olympic-level athletes and sedentary controls. Resting serum samples were collected from male and female marathon runners and weightlifters (with 5-15 years of training), alongside age- and sex-matched sedentary individuals. Proteomic profiling was performed using tandem mass spectrometry. Data were processed with MaxQuant and analyzed using Perseus. Selected proteins were confirmed using antibody-based assays. Among 301 identified protein groups, 36 showed significant differences between groups. Apolipoprotein A-IV (APOA4) was elevated in athletes, particularly marathoners, suggesting cardiovascular adaptation to endurance training. Fibronectin 1 (FN1) was reduced in weightlifters, consistent with vascular remodeling associated with resistance training. Marathoners exhibited higher levels of von Willebrand factor (VWF) and glycosylphosphatidylinositol-specific phospholipase D1 (GPLD1), and lower levels of galectin-3-binding protein (LGAS3BP) and leucine-rich alpha-2-glycoprotein 1 (LRG1), indicating immunomodulatory effects of oxidative training. Weightlifters showed reduced levels of GPLD1 and extracellular matrix protein 1 (ECM1), reflecting distinct remodeling pathways. FN1, APOA4, VWF, LGALS3BP and ECM1 levels were further confirmed. Endurance and resistance training elicit modality-specific serum proteomic adaptations that reflect vascular, endothelial, and hemostatic remodeling. These molecular signatures, observed in both sexes, highlight stable changes induced by chronic training and may inform cardiovascular prevention strategies and evidence-based approaches in sports science to optimize training and performance. Show less

Based on data from the EUROASPIRE IV survey, we aimed at assessing the possible residual risk tracked by serum apolipoprotein B in coronary patients with elevated serum triglycerides. All samples from the total EUROASPIRE IV survey (n = 7998) with low serum total cholesterol (<4.5 mmol/L) and high serum triglycerides (≥1.7 mmol/L) were used to analyse apolipoprotein A-I (apoA-I) and apolipoprotein B (apoB) concentrations (n = 938). We selected a similar number of participants (n = 938) with low total cholesterol and with low triglycerides (<1.0 mmol/L). In addition, phospholipid transfer protein (PLTP) and cholesteryl ester transfer protein (CETP) as well as paraoxonase-1 (PON-1), angiopoietin-like (ANGPTL)-3 and ANGPTL-8 were analysed in randomly selected participants. Despite the lower low-density lipoprotein cholesterol (LDL-C) concentration in the patients with TG ≥ 1.7 mmol/L (1.89 ± 0.44 mmol/L) than those with TG < 1.0 mmol/L (1.99 ± 0.43 mmol/L), p < 0.0001), serum total cholesterol, apoB, and HbA1c were all significantly (p < 0.0001) higher in patients with TG ≥ 1.7 mmol/L. In addition, high-density lipoprotein cholesterol (HDL-C), apoA-I, and CETP activity were significantly lower (p < 0.001) in these patients. The prevalence of obesity and diabetes was higher in the participants with TG ≥ 1.7 mmol/L than in those with TG < 1.0 mmol/L (52.6 % vs 21.9 % and 41.3 % vs. 20.0 %). Statin treatment is mainly decreasing serum LDL-C concentration, but apoB measurements with excess serum triglycerides carried by apoB-containing lipoproteins could provide more specific information about the risk assessment of cardiovascular disease in atherogenic dyslipidemia. Show less

Lipoprotein(a) [Lp(a)] is a genetically determined, proatherogenic, and prothrombotic lipoprotein associated with an increased risk of atherosclerotic cardiovascular disease (ASCVD). Elevated Lp(a) levels are associated with progressive ASCVD even when guideline-recommended low-density lipoprotein cholesterol (LDL-C) targets are achieved under optimal lipid-lowering therapy. There is currently no approved pharmacological therapy specifically targeting Lp(a) reduction in routine clinical practice; therefore, current management strategies for patients with elevated Lp(a) primarily focus on aggressive control of modifiable cardiovascular risk factors and intensive LDL-C lowering. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors provide a modest reduction in Lp(a) levels and have been associated with greater cardiovascular benefit in patients with high baseline Lp(a); however, this degree of reduction is often insufficient in individuals with markedly elevated Lp(a) levels and progressive ASCVD. At present, lipoprotein apheresis remains the only therapeutic option capable of achieving substantial and sustained reductions in Lp(a) concentrations and is recommended in selected high-risk patients with progressive ASCVD despite optimal medical therapy. Meanwhile, Lp(a)-specific therapies, including antisense oligonucleotides and small interfering RNA agents, are in advanced clinical development and have shown marked reductions in Lp(a) levels in early phase trials. These emerging therapies are expected to significantly change future treatment strategies for patients with Lp(a)-driven residual cardiovascular risk. Show less