Mitochondrial stress: a bridge between mitochondrial dysfunction and metabolic diseases?

Cell Signal. 2011 Oct;23(10):1528-33. doi: 10.1016/j.cellsig.2011.05.008. Epub 2011 May 15.


Under pathophysiological conditions such as obesity, excessive oxidation of nutrients may induce mitochondrial stress, leading to mitochondrial unfolded protein response (UPR(mt)) and initiation of a retrograde stress signaling pathway. Defects in the UPR(mt) and the retrograde signaling pathways may disrupt the integrity and homeostasis of the mitochondria, resulting in endoplasmic reticulum stress and insulin resistance. Improving the capacity of mitochondria to reduce stress may be an effective approach to improve mitochondria function and to suppress obesity-induced metabolic disorders such as insulin resistance and type 2 diabetes.

Publication types

  • Review

MeSH terms

  • Endoplasmic Reticulum / metabolism
  • Homeostasis
  • Humans
  • Insulin Resistance
  • Membrane Potential, Mitochondrial
  • Metabolic Diseases / physiopathology*
  • Mitochondria / metabolism
  • Mitochondria / physiology*
  • Mitochondrial Proteins / metabolism
  • Molecular Chaperones / metabolism
  • Oxidative Phosphorylation
  • Peptide Hydrolases / metabolism
  • Protein Folding
  • Signal Transduction*
  • Unfolded Protein Response*


  • Mitochondrial Proteins
  • Molecular Chaperones
  • Peptide Hydrolases