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Analyzing Supercomplexes of the Mitochondrial Electron Transport Chain with Native Electrophoresis, In-gel Assays, and Electroelution
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Metformin Targets Mitochondrial Electron Transport to Reduce Air-Pollution-Induced Thrombosis

Saul Soberanes1, Alexander V Misharin1, Amit Jairaman2

  • 1Department of Medicine and Pulmonary and Critical Care Medicine, Northwestern University, 240 E Huron Street, M300, Chicago, IL 60611, USA.

Cell Metabolism
|October 16, 2018
PubMed

Insights

Metformin protects against air pollution effects. It prevents inflammation and thrombosis linked to particulate matter by inhibiting mitochondrial reactive oxygen species and calcium release-activated channels in macrophages.

Area of Science:

  • Environmental Health
  • Toxicology
  • Pharmacology

Background:

  • Urban particulate matter (PM) air pollution is a significant health concern.
  • PM exposure triggers pro-inflammatory responses, including interleukin-6 (IL-6) release from alveolar macrophages.
  • This inflammation is linked to increased thrombosis risk.

Purpose of the Study:

  • To investigate the protective effects of metformin against PM-induced inflammation and thrombosis.
  • To elucidate the underlying molecular mechanisms of metformin's action.

Main Methods:

  • Murine models of PM air pollution exposure.
  • Treatment of mice and isolated murine/human alveolar macrophages with metformin.
  • Assessment of mitochondrial reactive oxygen species (ROS) generation, calcium release-activated channel (CRAC) activity, IL-6 release, and arterial thrombosis acceleration.
  • Genetic deletion of electron transport or CRAC channels in alveolar macrophages.

Main Results:

  • Metformin treatment prevented PM-induced generation of complex III mitochondrial ROS.
  • This inhibition of ROS was necessary for preventing CRAC channel opening and IL-6 release.
  • Targeted genetic deletion of electron transport or CRAC channels in alveolar macrophages abrogated PM-induced thrombosis acceleration.

Conclusions:

  • Metformin demonstrates protective effects against PM-induced inflammation and thrombosis in a murine model.
  • The mechanism involves the inhibition of mitochondrial ROS and CRAC channel-mediated IL-6 release.
  • Metformin represents a potential therapeutic strategy to mitigate health risks associated with air pollution exposure.
Keywords:
air pollutioncalcium channelselectron transport chainmitochondriaproteostasisreactive oxygen speciessignalingthrombosis

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