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Ac-SDKP modulates apoptosis via HSP27 and the FAS/FASL and mitochondrial axes

Wenxin Guo1,2, Jinyin Yan3, Wenli Li1,2

  • 1School of Basic Medical Sciences, North China University of Science and Technology, Tangshan, China.

Animal Models and Experimental Medicine
|August 6, 2026
PubMed
Abstract

Insights

The anti-fibrotic tetrapeptide Ac-SDKP modulates apoptosis via heat shock protein 27 (HSP27) in silicosis. Targeting HSP27 may restore apoptotic-fibrotic balance in lung fibrosis.

Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Fibrotic Lung Disease Research

Background:

  • Silicosis is a progressive lung fibrosis from crystalline silica exposure.
  • The anti-fibrotic tetrapeptide Ac-SDKP shows therapeutic potential.
  • Mechanisms of Ac-SDKP in silica-induced lung injury, particularly HSP27's role in apoptosis, require clarification.

Purpose of the Study:

  • Investigate Ac-SDKP's modulation of apoptosis in silicosis.
  • Elucidate the role of heat shock protein 27 (HSP27) in this process.
  • Explore therapeutic strategies targeting HSP27 for pulmonary fibrosis.

Main Methods:

  • In vivo studies using Wistar rats with silica exposure, treated with Ac-SDKP.
  • In vitro experiments with MEF and A549 cells treated with TGF-β1 and Ac-SDKP.
  • Utilized HSP27 interference vectors to assess apoptosis pathways (FAS/FASL, mitochondrial).

Main Results:

  • Ac-SDKP alleviated pulmonary fibrosis and reduced apoptosis in vivo.
  • In vitro, Ac-SDKP restored apoptosis suppressed by TGF-β1 via HSP27-mediated pathways.
  • HSP27 knockdown enhanced apoptosis and reduced fibrosis in vivo, confirming its anti-apoptotic role.

Conclusions:

  • Ac-SDKP context-dependently modulates apoptosis via HSP27.
  • HSP27 protects lung cells in vivo but promotes survival in vitro.
  • Targeting HSP27 offers a potential therapeutic strategy for silicosis and related fibrotic disorders.
Keywords:
FAS/FASL pathwayHSP27apoptosismitochondriasilicosis

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