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ROS-mediated lysosomal membrane permeabilization and autophagy inhibition regulate bleomycin-induced cellular

Zhangyang Qi1, Weiqi Yang1, Baibing Xue2

  • 1Department of Orthopaedics, Qilu Hospital, Shandong University Centre for Orthopaedics, Advanced Medical Research Institute, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.

Autophagy
|May 19, 2024
PubMed
Summary

Bleomycin-induced reactive oxygen species (ROS) impair autophagy by causing lysosomal damage, leading to cellular senescence. Targeting the autophagy-lysosome pathway may mitigate bleomycin

Keywords:
AutophagyROSbleomycincellular senescencelysosomal membrane permeabilization

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Pharmacology

Background:

  • Bleomycin is an effective chemotherapy drug with significant side effects, including pulmonary fibrosis and neurotoxicity.
  • The role of macroautophagy/autophagy in bleomycin's effects is recognized, but the underlying mechanisms are not fully understood.

Purpose of the Study:

  • To investigate the role of reactive oxygen species (ROS) in bleomycin-induced autophagy dysfunction.
  • To elucidate the relationship between autophagy defects and bleomycin-induced cellular senescence.

Main Methods:

  • Investigated the impact of bleomycin on autophagy flux and lysosomal function in vitro and in vivo.
  • Utilized N-acetylcysteine (NAC) to deplete ROS and assess its effects on bleomycin-induced phenotypes.
  • Examined the temporal relationship between lysosomal membrane permeabilization (LMP), autophagy blockage, and cellular senescence.

Main Results:

  • Bleomycin-induced ROS cause lysosomal membrane permeabilization (LMP), disrupting autophagy flux and lysosomal degradation.
  • N-acetylcysteine (NAC) treatment reversed LMP and autophagy defects.
  • LMP and autophagy inhibition preceded bleomycin-induced cellular senescence, suggesting a regulatory role for autophagy.

Conclusions:

  • Bleomycin-induced ROS play a critical role in impairing autophagic degradation and regulating cellular senescence.
  • The autophagy-lysosome degradation pathway represents a potential therapeutic target for modulating bleomycin's efficacy and reducing its side effects.