Do mitochondria age?

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.

FULL TEXT: Gerontology

Mitophagy

Mitophagy in cellular homeostasis

Pathogenic protein species implicated in neurodegenerative diseases (e.g., alpha synuclein, beta amyloid, tau, and TDP43) can associate with mitochondria and drive mitochondrial dysfunction.

Mitophagy, the process by which cells clear their damaged mitochondria, plays an important protective role in these circumstances: not only is the normal, healthy mitochondrial pool restored, but the proteotoxic species are cleared along with the bad mitochondria.

Mitokinin’s scientists have shown that by potentiating the PINK1 pathway in times of proteotoxic stress, neuron health can be restored and disease-driving pathologies reduced or eliminated.

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