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Program‐like aging and mitochondria: Instead of random damage by free radicals
Author(s) -
Blagosklonny Mikhail V.
Publication year - 2007
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.21602
Subject(s) - mitochondrion , autophagy , microbiology and biotechnology , cell , programmed cell death , senescence , biology , chemistry , biochemistry , apoptosis
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. J. Cell. Biochem. 102: 1389–1399, 2007. © 2007 Wiley‐Liss, Inc.