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PGC1α inhibits SiO2-induced fibrosis by regulating the mitochondrial respiratory chain

Shupeng Liu1, Yue Zhang1, Hongli Wang1

  • 1School of Public Health, North China University of Science and Technology, Tangshan, Hebei, 063210, China.

Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association
|July 3, 2025
PubMed

Insights

Silicosis fibrosis, caused by silica particle inhalation, involves mitochondrial dysfunction. Increasing PGC1α expression ameliorates this damage, offering a potential therapeutic strategy for this lung disease.

Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Toxicology

Background:

  • Silicosis is a severe lung fibrotic disease with no effective treatment.
  • Inhaled silica particles (SiO2) trigger inflammatory responses and fibrosis.
  • Mitochondrial dysfunction in macrophages is implicated in silica-induced lung injury.

Purpose of the Study:

  • To investigate the role of PGC1α in silica-induced lung fibrosis.
  • To explore PGC1α's impact on macrophage mitochondrial function and fibroblast activity.
  • To identify PGC1α as a potential therapeutic target for silicosis.

Main Methods:

  • Studied PGC1α expression in silica-exposed macrophages.
  • Assessed mitochondrial respiratory chain function.
  • Evaluated the effect of PGC1α overexpression on SiO2-induced fibrosis in fibroblasts.

Main Results:

  • Silica exposure reduced PGC1α expression, impaired mitochondrial respiration, and enhanced fibroblast fibrosis.
  • Overexpression of PGC1α improved mitochondrial function and mitigated silica-induced fibrosis.
  • PGC1α demonstrated a protective role against silica-induced lung damage.

Conclusions:

  • PGC1α plays a critical role in regulating mitochondrial respiratory chain function in silicosis.
  • Increasing PGC1α expression can ameliorate mitochondrial damage and inhibit silicosis fibrosis.
  • PGC1α represents a promising therapeutic target for treating silicosis.
Keywords:
FibrosisMitochondrial respiratory chainPGC1αSilicosis

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