# TRPV1 in Cardiovascular Disease: A Molecular Nexus of Treatment

**Authors:** Qi Lu, Xiaoqing Ding, Binghong Gao

PMC · DOI: 10.3390/biom16030344 · Biomolecules · 2026-02-25

## TL;DR

This review explores how TRPV1, a protein channel, influences heart disease and could lead to new treatments.

## Contribution

The paper provides a comprehensive analysis of TRPV1's dual roles in cardiovascular disease pathophysiology and therapeutic potential.

## Key findings

- TRPV1 is involved in multiple cardiovascular diseases through various signaling pathways.
- TRPV1 has both protective and harmful effects depending on the disease context.
- Modulating TRPV1 signaling could offer new treatment strategies for CVD.

## Abstract

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.

## Linked entities

- **Genes:** TRPV1 (transient receptor potential cation channel subfamily V member 1) [NCBI Gene 7442]
- **Proteins:** TRPV1 (transient receptor potential cation channel subfamily V member 1), CALCA (calcitonin related polypeptide alpha), TFF2 (trefoil factor 2), NOS3 (nitric oxide synthase 3), Nos1 (nitric oxide synthase 1, neuronal)
- **Diseases:** myocardial infarction (MONDO:0005068), ischemia–reperfusion injury (MONDO:0005203), heart failure (MONDO:0005252), diabetes (MONDO:0005015), cardiovascular disease (MONDO:0004995)

## Full-text entities

- **Genes:** NOS3 (nitric oxide synthase 3) [NCBI Gene 4846] {aka EC-NOS, ECNOS, MYMY8, NOSIII, cNOS, eNOS}, CALCA (calcitonin related polypeptide alpha) [NCBI Gene 796] {aka CALC1, CGRP, CGRP-I, CGRP-alpha, CGRP1, CT}, TRPV1 (transient receptor potential cation channel subfamily V member 1) [NCBI Gene 7442] {aka VR1}
- **Diseases:** heart failure (MESH:D006333), hypertension (MESH:D006973), inflammation (MESH:D007249), cardiac remodeling (MESH:D020257), myocardial infarction (MESH:D009203), CVD (MESH:D002318), diabetes (MESH:D003920), reperfusion injury (MESH:D015427), ischemia (MESH:D007511)
- **Chemicals:** NO (MESH:D009614)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC13024381/full.md

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13024381/full.md

## References

83 references — full list in the complete paper: https://tomesphere.com/paper/PMC13024381/full.md

---
Source: https://tomesphere.com/paper/PMC13024381