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Abstract
The biological basis of human aging remains one of the greatest unanswered scientific questions. Increasing evidence, however, points to a role for alterations in mitochondrial function as a potential central regulator of the aging process. Here, we focus primarily on three aspects of mitochondrial biology that link this ancient organelle to how and why we age. In particular, we discuss the role of mitochondria in regulating the innate immune system, the mechanisms linking mitochondrial quality control to age-dependent pathology, and the possibility that mitochondrial-to-nuclear signaling might regulate the rate of aging.
Authors
Ji Yong Jang, Arnon Blum, Jie Liu, Toren Finkel
Figure 2
Aging impairs mitophagic removal of stressed mitochondria.
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The age-dependent decline in mitophagy might provide the mechanism to explain the known interrelationship between increased ROS, decreased bioenergetic capacity, and age-dependent functional decline. Agents such as spermidine and urolithin A appear to stimulate mitophagy and thereby prevent age-related pathologies, which are described in more detail in the main text.
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Copyright © 2019 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)
Copyright © 2019 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)