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Updated: May 31, 2025

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TWEAK/Fn14 axis may promote vascular smooth muscle cell senescence via p38 signaling pathway: preliminary evidence

Chunyang Wei1, Xiaoying Liu1, Zhuang Miao2

  • 1Department of Gerontology, the First Affiliated Hospital, Dalian Medical University, Dalian, China.

Future Science OA
|January 22, 2025
PubMed
Abstract

Insights

The TWEAK/Fn14 pathway promotes vascular smooth muscle cell (VSMC) senescence. This axis activates the p38 pathway, increasing senescence markers like SA-β-gal and P53 expression in VSMCs.

Area of Science:

  • Cardiovascular Biology
  • Cellular Senescence
  • Molecular Signaling

Background:

  • Vascular smooth muscle cell (VSMC) senescence contributes to cardiovascular disease.
  • The role of specific molecular pathways in VSMC senescence requires further elucidation.

Purpose of the Study:

  • To investigate the impact of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor-inducible 14 (Fn14) on VSMC senescence.
  • To assess the involvement of the p38 phosphorylation pathway in TWEAK-induced VSMC senescence.

Main Methods:

  • Established a rat arterial VSMC senescence model using angiotensin II.
  • Evaluated the effects of TWEAK and Fn14 on senescent VSMCs.
  • Assessed p38 phosphorylation pathway activation.

Main Results:

  • TWEAK and Fn14 expression were significantly elevated in senescent VSMCs.
  • TWEAK activated the p38 phosphorylation pathway.
  • TWEAK promoted SA-β-gal staining and P53 expression, indicating increased senescence.

Conclusions:

  • The TWEAK/Fn14 axis plays a significant role in promoting VSMC senescence.
  • The p38 phosphorylation pathway is involved in TWEAK-mediated VSMC senescence.
Keywords:
Fn14TWEAKVSMCsenescencevascular

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