Mitochondria and the autophagy-inflammation-cell death axis in organismal aging Review uri icon

Overview

MeSH Major

  • Aging
  • Autophagy
  • Cell Death
  • Inflammation
  • Mitochondria

abstract

  • Alterations of mitochondrial functions are linked to multiple degenerative or acute diseases. As mitochondria age in our cells, they become progressively inefficient and potentially toxic, and acute damage can trigger the permeabilization of mitochondrial membranes to initiate apoptosis or necrosis. Moreover, mitochondria have an important role in pro-inflammatory signaling. Autophagic turnover of cellular constituents, be it general or specific for mitochondria (mitophagy), eliminates dysfunctional or damaged mitochondria, thus counteracting degeneration, dampening inflammation, and preventing unwarranted cell loss. Decreased expression of genes that regulate autophagy or mitophagy can cause degenerative diseases in which deficient quality control results in inflammation and the death of cell populations. Thus, a combination of mitochondrial dysfunction and insufficient autophagy may contribute to multiple aging-associated pathologies.

publication date

  • August 26, 2011

Research

keywords

  • Review

Identity

Language

  • eng

PubMed Central ID

  • PMC3405151

Digital Object Identifier (DOI)

  • 10.1126/science.1201940

PubMed ID

  • 21868666

Additional Document Info

start page

  • 1109

end page

  • 12

volume

  • 333

number

  • 6046