“Mitochondrial Dysfunction in Cell Senescence and Aging”, Satomi Miwa, Sonu Kashyap, Eduardo Chini, Thomas von Zglinicki2022-07-01 (senolytics)⁠:

mitochondrial dysfunction and cell senescence are hallmarks of aging and are closely interconnected. Mitochondrial dysfunction, operationally defined as a decreased respiratory capacity per mitochondrion together with a decreased mitochondrial membrane potential, typically accompanied by increased production of oxygen free radicals, is a cause and a consequence of cellular senescence and figures prominently in multiple feedback loops that induce and maintain the senescent phenotype.

Here, we summarize pathways that cause mitochondrial dysfunction in senescence and aging and discuss the major consequences of mitochondrial dysfunction and how these consequences contribute to senescence and aging.

We also highlight the potential of senescence-associated mitochondrial dysfunction as an antiaging and anti-senescence intervention target, proposing the combination of multiple interventions converging onto mitochondrial dysfunction as novel, potent senolytics.

[Reason: “The interesting part of this paper is the discussion of mitochondrial function as a target to reduce the burden of senescence cells, either by preventing cells from becoming senescent, reducing the harmful signals secreted by senescent cells, or forcing these errant cells to self-destruct.”]