Mitohormesis and Inflammation

Previous Science Note

This article focusing on how both drug-induced and lipopolysaccharide (LPS)-induced mitochondrial stress in macrophages triggers a stress response called mitohormesis. Mitohormesis serves as a negative feedback mechanism to restrain inflammation. These findings have the potential to contribute to the development of novel strategies for counteracting acute and chronic inflammation by leveraging the Mitochondria-ROS stress response.

Mitohormesis reprogrammes macrophage metabolism to enforce tolerance

Click here for the original article: Greg A. Timblin, et. al., nature metabolism (2021)

Point of Interest

  • - Mitochondrial stress response, mitohormesis, occurs as macrophages transition from an LPS-responsive to LPS-tolerant state, with impaired pro-inflammatory gene transcription.
  • - Hydroxyoestrogen-triggered mitohormesis also suppresses mitochondrial oxidative metabolism and acetyl-CoA production enforcing an LPS-tolerant state.
  • - Mitochondrial ROS and mitochondrial reactive electrophilic species are TLR-dependent signaling molecules that activate mitohormesis as a negative feedback mechanism to control inflammation through tolerance.
Related Techniques
Total ROS detection
Higher sensitivity or for long-term live cell imaging HOT
Mitochondrial superoxide detection
MitoBright ROS - Mitochondrial Superoxide Detection
Glycolysis/Oxidative phosphorylation Assay
Glycolysis/OXPHOS Assay Kit
Glycolysis-related metabolites assay
Glucose and Lactate ​Assay Kit
Oxygen consumption rate assay
Extracellular OCR Plate Assay Kit
Mitochondrial membrane potential detection
JC-1 MitoMP Detection Kit / MT-1 MitoMP Detection Kit
Lysosomal function assay
Lysosomal pH and mass detection Kit HOT
Autophagy detection
DAPGreen / DAPRed (Autophagosome detection), DALGreen (Autolysosome detection)​

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