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Peer-reviewedCC BY-NCChannels (Austin, Tex.)

Potential roles for transient receptor potential vanilloid 1 in heart failure with preserved ejection fraction.

  • Zhicheng Gao1
  • Jiaqi Bao2
  • Chaojie He1
  • Haihua Pan1
  • Hao Zhang3
  • Changlin Zhai1
  1. 1Department of Cardiology, the First Hospital of Jiaxing, Affiliated Hospital of Jiaxing University, Jiaxing City, Zhejiang Province, China.
  2. 2Department of General Practice, the First Hospital of Jiaxing, Affiliated Hospital of Jiaxing University, Jiaxing City, Zhejiang Province, China.
  3. 3Vascular Outpatient Clinic, Heart and Vascular Center Rhein-Nahe-Pfalz, Bad Kreuznach, Germany.
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Abstract

Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome in which diastolic dysfunction develops against a background of interacting mechanisms: inflammation, oxidative stress, impaired calcium homeostasis, myocardial fibrosis, coronary microvascular dysfunction, mitochondrial impairment, and neurohumoral activation. Effective mechanism-targeted therapies remain limited. Transient receptor potential vanilloid 1 (TRPV1) is a nonselective cation channel expressed in cardiac sensory nerves, vascular endothelial cells, immune cells, and possibly other cardiovascular cell populations. It responds to diverse physical and chemical stimuli and may influence calcium handling, inflammatory signaling, oxidative stress, myocardial fibrosis, mitophagy, and ferroptosis. Preclinical studies have linked altered TRPV1 expression or activity to myocardial remodeling, impaired relaxation, microvascular dysfunction, and heart failure progression, but direct evidence in HFpEF is still sparse. This review summarizes the biological properties of TRPV1, considers how its signaling might intersect with HFpEF pathophysiology, reviews experimental TRPV1-targeted interventions, and identifies the evidence needed before TRPV1 can be evaluated as a potential therapeutic target.

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Cite

BibTeXRIS
BibTeX
@article{gao2026potential,
  title = {{Potential roles for transient receptor potential vanilloid 1 in heart failure with preserved ejection fraction.}},
  author = {Zhicheng Gao and Jiaqi Bao and Chaojie He and Haihua Pan and Hao Zhang and Changlin Zhai},
  journal = {Channels (Austin, Tex.)},
  year = {2026},
  month = oct,
  doi = {10.1080/19336950.2026.2746860},
  url = {https://europepmc.org/article/MED/42902773},
  note = {CC BY-NC},
}
RIS
TY  - JOUR
TI  - Potential roles for transient receptor potential vanilloid 1 in heart failure with preserved ejection fraction.
AU  - Zhicheng Gao
AU  - Jiaqi Bao
AU  - Chaojie He
AU  - Haihua Pan
AU  - Hao Zhang
AU  - Changlin Zhai
PY  - 2026
DA  - 2026/10/21
JO  - Channels (Austin, Tex.)
DO  - 10.1080/19336950.2026.2746860
UR  - https://europepmc.org/article/MED/42902773
AB  - Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome in which diastolic dysfunction develops against a background of interacting mechanisms: inflammation, oxidative stress, impaired calcium homeostasis, myocardial fibrosis, coronary microvascular dysfunction, mitochondrial impairment, and neurohumoral activation. Effective mechanism-targeted therapies remain limited. Transient receptor potential vanilloid 1 (TRPV1) is a nonselective cation channel expressed in cardiac sensory nerves, vascular endothelial cells, immune cells, and possibly other cardiovascular cell populations. It responds to diverse physical and chemical stimuli and may influence calcium handling, inflammatory signaling, oxidative stress, myocardial fibrosis, mitophagy, and ferroptosis. Preclinical studies have linked altered TRPV1 expression or activity to myocardial remodeling, impaired relaxation, microvascular dysfunction, and heart failure progression, but direct evidence in HFpEF is still sparse. This review summarizes the biological properties of TRPV1, considers how its signaling might intersect with HFpEF pathophysiology, reviews experimental TRPV1-targeted interventions, and identifies the evidence needed before TRPV1 can be evaluated as a potential therapeutic target.
SN  - 1933-6950
SN  - 1933-6969
ER  -