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.

线粒体质量和活性的下降与正常衰老有关，并与多种与年龄相关的疾病的发生有关。在这里，我们回顾了线粒体衍生肽水平下降导致衰老和与年龄相关的疾病的证据。我们特别讨论了线粒体衍生肽、护脑素和 MOTS-c 如何促进衰老过程的特定方面，包括细胞衰老、慢性炎症和认知能力下降。还回顾了与年龄相关疾病相关的 humanin 和 MOTS-c 编码区的遗传变异，特别强调线粒体变异如何反过来调节 MDP 表达和年龄相关表型。综上所述，这些观察结果表明线粒体衍生肽影响或调节衰老的许多关键方面，并且针对增加线粒体衍生肽水平的策略可能具有广泛的有益作用。