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The role of mitochondrial dysfunction in macrophages on SiO2 -induced pulmonary fibrosis: A review

Jia-Hui Zhao1,2, Shuang Li2,3, Shu-Ling Du1,2

  • 1Weifang Medical University, Weifang, Shandong, China.

Journal of Applied Toxicology : JAT
|July 19, 2023
PubMed

Insights

Silica dust causes lung fibrosis by damaging mitochondria in macrophages. Targeting these damaged mitochondria may prevent or reduce silicosis severity.

Area of Science:

  • Pulmonary Medicine
  • Toxicology
  • Cell Biology

Background:

  • Mitochondrial dysfunction is implicated in silicosis pathogenesis.
  • Mechanisms linking silica exposure to mitochondrial damage and fibrosis require systematic review.

Purpose of the Study:

  • To elucidate how silica dust induces mitochondrial damage in macrophages.
  • To detail the role of silica-induced mitochondrial damage in pulmonary fibrosis.
  • To provide a comprehensive summary of these molecular events in silicosis.

Main Methods:

  • Literature review of epidemiologic and toxicological studies.
  • Analysis of molecular mechanisms of silica-induced mitochondrial abnormalities.
  • Examination of pathways through which damaged mitochondria contribute to pulmonary fibrosis.

Main Results:

  • Silica dust causes morphological and functional abnormalities in mitochondria.
  • Damaged mitochondria trigger molecular pathways leading to pulmonary fibrosis.
  • Mitochondrial abnormalities in alveolar macrophages are central to silicosis development.

Conclusions:

  • Silica-induced mitochondrial damage in macrophages is a key driver of silicosis.
  • Interventions targeting silica-damaged mitochondria could be therapeutic for silicosis.
  • Further research into these mechanisms can inform preventative strategies.
Keywords:
ROS: ATPmacrophage mitochondrial dysfunctionpulmonary fibrosissilicosis

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