Study summary · research use only
Mitochondrial-derived peptides in aging and age-related diseases
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review discusses evidence that a decline in mitochondrial-derived peptides contributes to aging and age-related disease, focusing on humanin and MOTS-c and their roles in cellular senescence, chronic inflammation, and cognitive decline. The authors describe genetic variations in the coding regions of humanin and MOTS-c associated with age-related diseases and discuss how mitochondrial variants might regulate mitochondrial-derived peptide expression and age-related phenotypes. The abstract states that these peptides are suggested to influence several aspects of aging and that strategies to increase their levels are described as having potential broad effects. Species and study type are not specified.
Abstract
A decline in mitochondrial quality and activity has been associated with normal aging and correlated with the development of a wide range of age-related diseases. Here, we review the evidence that a decline in the levels of mitochondrial-derived peptides contributes to aging and age-related diseases. In particular, we discuss how mitochondrial-derived peptides, humanin and MOTS-c, contribute to specific aspects of the aging process, including cellular senescence, chronic inflammation, and cognitive decline. Genetic variations in the coding region of humanin and MOTS-c that are associated with age-related diseases are also reviewed, with particular emphasis placed on how mitochondrial variants might, in turn, regulate MDP expression and age-related phenotypes. Taken together, these observations suggest that mitochondrial-derived peptides influence or regulate a number of key aspects of aging and that strategies directed at increasing mitochondrial-derived peptide levels might have broad beneficial effects.
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