Program-like aging and mitochondria: instead of random damage by free radicals.
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.
Blagosklonny
Mikhail V
MV
Cancer Center, Ordway Research Institute, 150 New Scotland Ave, and Oncotarget, Albany, New York 12208, USA. blagosklonny@oncotarget.com
D000375:Aging / Q000502:physiology*; D000818:Animals; D002453:Cell Cycle; D005609:Free Radicals / Q000378:metabolism*; D006801:Humans; D008928:Mitochondria / Q000502:physiology*; D008954:Models, Biological
D005609:Free Radicals