Journal
SCIENCE
Volume 333, Issue 6046, Pages 1109-1112Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1201940
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Funding
- NIH
- American Lebanese Syrian Associated Charities
- European Union (EU)
- Agence Nationale de la Recherche
- Association pour la Recherche sur le Cancer
- AXA Chair for Longevity Research
- Fondation pour la Recherche Medicale
- Institut National du Cancer
- Ligue Nationale Contre le Cancer
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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.
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