Evidence map›Paper›PMID 41897282›Full record

ReviewBiomolecules2026

TRPV1 in Cardiovascular Disease: A Molecular Nexus of Treatment.

Qi Lu, Xiaoqing Ding, Binghong Gao

Abstract readReview
In one paragraph

Review in Biomolecules, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Qi LuSchool of Exercise and Health, Shanghai University of Sport, Shanghai 200438, China.
Xiaoqing DingSchool of Athletic Performance, Shanghai University of Sport, Shanghai 200438, China.
Binghong GaoSchool of Athletic Performance, Shanghai University of Sport, Shanghai 200438, China.

Funding

Macao Polytechnic University No.RP/FCSD-02/2025National Natural Science Foundation of China No.31771316Shanghai Key Lab of Human Performance (Shanghai University of Sport) No.11DZ2261100
6 · The paper itself

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.

Indexed as

Cardiovascular DiseasesTRPV Cation ChannelsAnimalsHumansOxidative StressSignal TransductionTRPV1 protein, humanTRPV Cation Channelscardiac remodelingcardiovascular diseasediabetesheart failurehypertensionischemia–reperfusion injurymyocardial infarctionTRPV1

Identifiers

PMID41897282
PMCPMC13024381

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.