Open AccessMitochondrial-derived peptides in aging and age-related diseases
Author(s) -
SuJeong Kim,
Brendan Miller,
Hiroshi Kumagai,
Ana R. Silverstein,
Melanie Flores,
Kelvin Yen
Publication year - 2020
Publication title -
geroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.883
H-Index - 63
eISSN - 2509-2715
pISSN - 2509-2723
DOI - 10.1007/s11357-020-00262-5
Subject(s) - senescence , biology , mitochondrion , mitochondrial dna , phenotype , cognitive decline , ageing , bioinformatics , genetics , neuroscience , disease , medicine , gene , dementia
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.