title: Mitochondrial Aging: Is There a Mitochondrial Clock?
abstract: Fragmentation (fission) of mitochondria, occurring in response to oxidative challenge, leads to heterogeneity in the mitochondrial population. It is assumed that fission provides a way to segregate mitochondrial content between the "young" and "old" phenotype, with the formation of mitochondrial "garbage," which later will be disposed. Fidelity of this process is the basis of mitochondrial homeostasis, which is disrupted in pathological conditions and aging. The asymmetry of the mitochondrial fission is similar to that of their evolutionary ancestors, bacteria, which also undergo an aging process. It is assumed that mitochondrial markers of aging are recognized by the mitochondrial quality control system, preventing the accumulation of dysfunctional mitochondria, which normally are subjected to disposal. Possibly, oncocytoma, with its abnormal proliferation of mitochondria occupying the entire cytoplasm, represents the case when segregation of damaged mitochondria is impaired during mitochondrial division. It is plausible that mitochondria contain a "clock" which counts the degree of mitochondrial senescence as the extent of flagging (by ubiquitination) of damaged mitochondria. Mitochondrial aging captures the essence of the systemic aging which must be analyzed. We assume that the mitochondrial aging mechanism is similar to the mechanism of aging of the immune system which we discuss in detail.
authors.affiliation: Belozersky Institute of Physico-Chemical Biology.
authors.forename: Dmitry B
authors.initials: DB
authors.lastname: Zorov
authors.affiliation: Faculty of Bioengineering and Bioinformatics.
authors.forename: Vasily A
authors.initials: VA
authors.lastname: Popkov
authors.affiliation: International Laser Center.
authors.forename: Ljubava D
authors.initials: LD
authors.lastname: Zorova
authors.affiliation: Biological Faculty, Lomonosov Moscow State University, Russia.
authors.forename: Ivan A
authors.initials: IA
authors.lastname: Vorobjev
authors.affiliation: Belozersky Institute of Physico-Chemical Biology.
authors.forename: Irina B
authors.initials: IB
authors.lastname: Pevzner
authors.affiliation: Belozersky Institute of Physico-Chemical Biology.
authors.forename: Denis N
authors.initials: DN
authors.lastname: Silachev
authors.affiliation: Faculty of Bioengineering and Bioinformatics.
authors.forename: Savva D
authors.initials: SD
authors.lastname: Zorov
authors.affiliation: Belozersky Institute of Physico-Chemical Biology.
authors.forename: Stanislovas S
authors.initials: SS
authors.lastname: Jankauskas
authors.affiliation: Faculty of Bioengineering and Bioinformatics.
authors.forename: Valentina A
authors.initials: VA
authors.lastname: Babenko
authors.affiliation: Belozersky Institute of Physico-Chemical Biology.
authors.forename: Egor Y
authors.initials: EY
authors.lastname: Plotnikov
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D001343:Autophagy / Q000502:physiology; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D008136:Longevity / Q000502:physiology*; D063306:Mitophagy / Q000502:physiology*; D018384:Oxidative Stress / Q000502:physiology; D010641:Phenotype
keywords: Autophagy; Biology of aging; Cellular senescence; Mitochondria; Mitophagy