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.

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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