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Mitochondrial ROS-induced lysosomal dysfunction impairs autophagic flux and contributes to M1 macrophage polarization

Yujia Yuan1, Younan Chen1, Tianqing Peng2,3

  • 1Key Laboratory of Transplant Engineering and Immunology, NHFPC, and Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu, China.

Clinical Science (London, England : 1979)
|August 7, 2019
PubMed

Insights

High glucose impairs macrophage autophagy and mitochondrial function, promoting M1 polarization via reactive oxygen species (ROS). Antioxidant treatment blocking ROS can prevent this, offering insights into treating diabetic complications.

Area of Science:

  • Cell Biology
  • Immunology
  • Metabolism

Background:

  • Macrophage M1 polarization and inflammation are linked to diabetic complications.
  • Autophagy impairment worsens macrophage inflammation, but its regulation in hyperglycemia is unclear.

Purpose of the Study:

  • To investigate the regulation of macrophage autophagy under hyperglycemic conditions.
  • To elucidate the role of mitochondrial dysfunction and reactive oxygen species (ROS) in macrophage polarization during diabetes.

Main Methods:

  • Utilized streptozotocin (STZ)-induced diabetic mice and high glucose (HG)-stimulated RAW 264.7 cells.
  • Assessed autophagy-lysosome system and mitochondrial function.
  • Investigated the effects of Mito-TEMPO and Ndufs4 silencing on macrophage polarization and autophagic flux.

Main Results:

  • Hyperglycemia impairs the autophagy-lysosome system and mitochondrial function in macrophages.
  • Mitochondrial dysfunction increases ROS, blocking autophagic flux and promoting M1 polarization.
  • Inhibiting mitochondrial ROS with Mito-TEMPO prevents M1 polarization, an effect reversed by blocking autophagic flux.

Conclusions:

  • Mitochondrial ROS are key mediators in promoting M1 macrophage polarization by disrupting the autophagy-lysosome system under hyperglycemic conditions.
  • Targeting mitochondrial ROS may offer a novel therapeutic strategy for diabetic complications.
Keywords:
autophagydiabeteslysosomemacrophage polarizationmitochondria

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