Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality worldwide, posing a significant and ongoing burden on healthcare systems. Early identification of reliable biomarkers is essential for improving risk stratification, diagnosis, and therapeutic monitoring. Serotonin (5-hydroxytryptamine, 5-HT) has recently emerged as a candidate biomarker implicated in early cardiovascular pathophysiological processes, including platelet activation, vascular smooth muscle cell dysfunction, endothelial impairment, and intraplaque inflammation. This narrative review synthesizes current evidence from peer-reviewed literature retrieved from major scientific databases, including MDPI, PubMed, Scopus, Web of Science, and Elsevier. Relevant studies were selected for their contributions to understanding the role of serotonin in cardiovascular physiology and pathology, with a focus on its potential utility as a biomarker. Serotonin exerts pleiotropic effects within the cardiovascular system, extending beyond its established role as a neurotransmitter. It plays a critical role in platelet aggregation, regulation of vascular tone, and vascular remodeling. Experimental and translational studies suggest that altered serotonin signaling is associated with endothelial dysfunction, atherogenesis, and thrombotic processes. These findings support that serotonin may have potential as a novel or adjunctive biomarker in cardiovascular disease. Although emerging evidence highlights the relevance of serotonin in cardiovascular pathophysiology, its clinical utility as a biomarker remains limited by insufficient large-scale clinical validation and lack of standardized measurement approaches. At present, serotonin should be considered an investigational biomarker. Further well-designed prospective studies are required to establish its diagnostic and prognostic value and to determine its applicability in routine clinical practice.

Cardiovascular disease (CVD) remains the leading cause of mortality worldwide, with aging as one of its main risk factors. Cellular senescence and oxidative stress form a bidirectional vicious cycle that drives vascular aging, endothelial dysfunction, and atherosclerotic progression. This state-of-the-art review synthesizes current evidence on the interplay between oxidative stress and senescence in cardiovascular aging and critically assesses whether antioxidant strategies can benefit vascular health. A targeted literature search was conducted in PubMed/MEDLINE, Web of Science, and Scopus (2016–2026). While endogenous antioxidant defenses decline with age, exogenous antioxidants, including resveratrol, vitamins C and E, omega-3 fatty acids, carotenoids, and coenzyme Q10,demonstrate promising preclinical effects, yet large-scale clinical trials have yielded inconsistent results. The VITAL and STRENGTH trials failed to demonstrate significant cardiovascular benefit with omega-3 supplementation, and elevated serum β-carotene was found paradoxically associated with increased cardiovascular mortality. Emerging mitochondria-targeted antioxidants (MitoQ, MitoTEMPO) show preclinical promise but require further clinical validation. Current evidence does not support antioxidant supplementation for cardiovascular prevention. Lifestyle interventions, particularly antioxidant-rich dietary patterns such as the Mediterranean diet, remain the safest strategy. Future research should develop personalized approaches guided by oxidative stress biomarkers and long-term trials.