Serotonin in Cardiovascular Disease: From Pathophysiological Insights to Clinical Utility

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.