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Updated: Jul 10, 2026

Imaging of mtHyPer7, a Ratiometric Biosensor for Mitochondrial Peroxide, in Living Yeast Cells
Published on: June 2, 2023
Program-like aging and mitochondria: instead of random damage by free radicals
1Cancer Center, Ordway Research Institute, 150 New Scotland Ave, and Oncotarget, Albany, New York 12208, USA. blagosklonny@oncotarget.com
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.
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