title: Mitochondria and the autophagy-inflammation-cell death axis in organismal aging.
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.
authors.affiliation: Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. douglas.green@stjude.org
authors.forename: Douglas R
authors.initials: DR
authors.lastname: Green
authors.forename: Lorenzo
authors.initials: L
authors.lastname: Galluzzi
authors.forename: Guido
authors.initials: G
authors.lastname: Kroemer
mesh_terms: D000375:Aging; D000818:Animals; D017209:Apoptosis; D001343:Autophagy; D016923:Cell Death; D016922:Cellular Senescence; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D008928:Mitochondria / Q000502:physiology*; D009336:Necrosis; D019636:Neurodegenerative Diseases / Q000503:physiopathology