ArticleScientific reports2026
Cardiovascular peptide markers are associated with age-related macular degeneration in the Bialystok PLUS general population cohort.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Age-related macular degeneration (AMD) and cardiovascular disease (CVD) share numerous risk factors; however, protein biomarkers for AMD are lacking. We investigated whether circulating cardiovascular peptide biomarkers are associated with AMD in the population-based Białystok PLUS cohort. This cross-sectional analysis included 699 participants aged ≥ 50 years (AMD + = 93; AMD⁻ = 606) examined between 2018 and 2023. AMD was graded from fundus photos with the use of the Wisconsin and modified International Classification systems. Ninety-two cardiovascular proteins were quantified in serum with the Olink Target Cardiovascular III panel. Age-adjusted linear or logistic regressions assessed biomarker-AMD associations, and receiver-operating-characteristic (ROC) curves evaluated discriminative performance. After adjustment, AMD+ participants exhibited lower galectin-4 (β = - 0.15, p = 0.043) and TNF-receptor-superfamily-member-10 C (TNFRSF10C) (β = - 0.17, p = 0.037) concentrations and higher von Willebrand factor (vWF) levels (β = 0.22, p = 0.036) versus AMD⁻ individuals. Galectin-4, TNFRSF10C, and vWF predicted AMD with areas under the ROC curve of 0.613 (95% confidence interval [CI] 0.516-0.709), 0.606 (0.520-0.692), and 0.594 (0.500-0.687), respectively. Optimal cut-offs were 4.05 NPX for galectin-4, 5.09 NPX for TNFRSF10C, and 8.03 NPX for vWF, yielding sensitivities/specificities of 57%/63%, 58%/62% and 55%/63%, respectively. Elevated vWF and reduced galectin-4 and TNFRSF10C are independently associated with AMD, suggesting overlapping vascular, inflammatory and apoptotic pathways with CVD. Incorporation of these peptides into risk-stratification algorithms could enhance early AMD detection and motivate mechanistic studies targeting the TRAIL-TNFRSF10C axis and galectin-mediated signaling.
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