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Updated: Nov 18, 2025

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro
Published on: February 15, 2022
TRPV1 activation inhibits phenotypic switching and oxidative stress in vascular smooth muscle cells by upregulating
Yi Zhou1, Xueli Wang1, Lu Guo2
1Department of Neurology, 980 Hospital of PLA Joint Logistics Support Forces, 398 ZhongShan Xi Road, QiaoXi District, ShiJiaZhuang, Hebei Province, China.
Abstract:
The proliferation and migration of vascular smooth muscle cells (VSMCs) is one of main reasons of vascular remodeling and is the pathogenesis of atherosclerosis and other vascular diseases. Transient receptor potential vanilloid 1 (TRPV1) is the specific receptor of capsaicin. TRPV1 has been previously reported to inhibit proliferation, migration and phenotypic switching, but the regulatory mechanisms and relevant signalling pathways are not clear. The aim of this study was to investigate the effects of capsaicin-activated TRPV1 on VSMC phenotypic switching. In this study, oxidized low density lipoprotein (ox-LDL) was used to induce the proliferation and migration of VSMCs. Our data showed that the VSMC proliferation induced by ox-LDL was dependent on the concentration of ox-LDL. Nevertheless, the data showed that capsaicin activated TRPV1 significantly decreased ox-LDL-induced superoxide anion generation. Phenotypic switching of VSMCs was inhibited by the activation of TRPV1. Furthermore, capsaicin decreased ox-LDL-induced superoxide anion generation by activating peroxisome proliferator activated receptor α (PPARα). TRPV1 inhibited VSMC phenotypic switching via upregulated expression of PPARα. It may be considered a useful target for the treatment of vascular remodeling.
Insights
Capsaicin-activated Transient Receptor Potential Vanilloid 1 (TRPV1) inhibits vascular smooth muscle cell (VSMC) proliferation and phenotypic switching. This occurs by reducing superoxide generation and upregulating peroxisome proliferator activated receptor α (PPARα), suggesting a therapeutic target for vascular remodeling.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Cellular Physiology
Background:
- Vascular smooth muscle cell (VSMC) proliferation and migration drive vascular remodeling and diseases like atherosclerosis.
- The role and regulatory mechanisms of Transient Receptor Potential Vanilloid 1 (TRPV1) in VSMC function remain unclear.
Purpose of the Study:
- To investigate the effects of capsaicin-activated TRPV1 on VSMC phenotypic switching.
- To elucidate the signaling pathways involved in TRPV1-mediated regulation of VSMCs.
Main Methods:
- Oxidized low-density lipoprotein (ox-LDL) was used to induce VSMC proliferation and migration in vitro.
- The impact of capsaicin-activated TRPV1 on superoxide anion generation and VSMC phenotypic switching was assessed.
- The role of peroxisome proliferator activated receptor α (PPARα) in TRPV1 signaling was investigated.
Main Results:
- Ox-LDL induced VSMC proliferation in a dose-dependent manner.
- Capsaicin-activated TRPV1 significantly reduced ox-LDL-induced superoxide anion generation.
- TRPV1 activation inhibited VSMC phenotypic switching, partly via upregulation of PPARα expression.
- Capsaicin decreased ox-LDL-induced superoxide anion generation by activating PPARα.
Conclusions:
- Capsaicin-activated TRPV1 inhibits VSMC phenotypic switching and proliferation.
- TRPV1 exerts its effects by modulating superoxide anion generation and upregulating PPARα.
- TRPV1 activation represents a potential therapeutic strategy for vascular remodeling and related diseases.
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