Catestatin as a Marker of Cardiovascular Diseases

Catestatin (CST), a 21-amino acid peptide derived from Chromogranin A, is a potent endogenous inhibitor of catecholamine release and a key regulator of sympathovagal balance essential for cardiovascular homeostasis. Given its multifaceted physiological role, CST has emerged as a promising biomarker for hypertensive and ischemic disorders. This review synthesizes current evidence on CST dynamics and its mechanistic involvement in disease progression.

Following PRISMA 2020 guidelines, a systematic search of PubMed/MEDLINE and eLibrary.ru was conducted through October 2025. From 339 identified records, original clinical and experimental studies on CST biology, cardiovascular physiology, and its role in hypertension and coronary artery disease were selected.

CST is a stage-specific marker; its elevation reflects adaptive responses in early-stage disease, while systemic depletion predicts advanced target organ damage and adverse clinical outcomes. This dynamic profile, influenced by genetic and metabolic variability, establishes CST as a possible tool for risk stratification and monitoring progression in hypertensive and ischemic populations.

Current evidence for the mechanistic role of CST in cardiovascular diseases remains predominantly preclinical, with clinical studies often limited by small cohorts and heterogeneous methodologies. Despite these constraints, emerging data position CST as an indicator of autonomic and structural deterioration. Addressing existing inconsistencies in clinical findings is essential for validating CST as a standardized tool for cardiovascular risk assessment.

Further large-scale longitudinal studies are warranted to standardize CST measurement protocols and validate its clinical utility as a prognostic biomarker in cardiovascular medicine.