Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality worldwide, necessitating a deeper understanding of novel regulatory mechanisms and therapeutic targets. Transient receptor potential vanilloid subtype 1 (TRPV1), a non-selective cation channel extensively expressed in the cardiovascular system, has been implicated in the pathogenesis and progression of various CVDs, including myocardial infarction, ischemia–reperfusion injury, adverse cardiac remodeling, heart failure, hypertension, and diabetes. Recent studies demonstrate that TRPV1 modulates key signaling pathways associated with inflammation, oxidative stress, mitochondrial function, and apoptosis, exerting both protective and detrimental effects depending on specific disease contexts and experimental conditions. The dual regulatory roles of TRPV1, mediated through pathways such as TRPV1/CGRP/SP and TRPV1/eNOS/NO, underline its complexity and clinical relevance. This review summarizes current findings on the expression and function of TRPV1 in diverse cardiovascular tissues and models, critically evaluates its role in CVD pathophysiology, and discusses the therapeutic potential of modulating TRPV1-associated signaling. Understanding these mechanisms may provide valuable insights into developing precise intervention strategies against cardiovascular diseases.
Lu et al. (Wed,) studied this question.
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