title: Program-like aging and mitochondria: instead of random damage by free radicals.
abstract: As recently suggested, the target of rapamycin (TOR) pathway, rather than molecular damage by free radicals, drives aging and diseases of aging. But may mitochondria nevertheless contribute to aging? Here, I discuss aimless program-like aging (versus altruistic program), conflict between the cell and mitochondria, cell murder (versus cell suicide) and the role of mitochondria in aging. In particular, life-long selection among mitochondria may yield "selfish" (malignant) mitochondria resistant to autophagy. And TOR may create an intra-cellular environment that is permissive for such selfish mitochondria. In theory, pharmacologic inhibitors of the TOR pathway may reverse accumulation of defective mitochondria, while also inhibiting the aging process.
authors.affiliation: Cancer Center, Ordway Research Institute, 150 New Scotland Ave, and Oncotarget, Albany, New York 12208, USA. blagosklonny@oncotarget.com
authors.forename: Mikhail V
authors.initials: MV
authors.lastname: Blagosklonny
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D002453:Cell Cycle; D005609:Free Radicals / Q000378:metabolism*; D006801:Humans; D008928:Mitochondria / Q000502:physiology*; D008954:Models, Biological
chemical_list: D005609:Free Radicals