Mitochondrial-derived peptides in aging and age-related diseases — VialBase Research
high
- MOTS-c and humanin decline with aging
- MDPs regulate mitochondrial function and cellular stress responses
- MOTS-c supplementation may counteract age-related metabolic decline
Summary
Review from the Cohen lab (MOTS-c discoverers) examining how mitochondrial-derived peptides (MDPs), including MOTS-c and humanin, change with aging and contribute to age-related diseases. The paper frames MDPs as a new class of aging biomarkers and potential therapeutic targets.
Key Findings
- MOTS-c and humanin plasma levels decline with advancing age
- MDPs regulate mitochondrial function, cellular stress responses, and metabolism
- MOTS-c acts as a retrograde signal from mitochondria to the nucleus
- Age-related MDP decline correlates with metabolic dysfunction and sarcopenia
- MOTS-c supplementation restores youthful metabolic phenotype in aged mice
- MDPs represent a new axis of the mitochondrial theory of aging
Methodology
Review synthesizing preclinical and early clinical data on mitochondrial-derived peptides in the context of aging biology. Covers MOTS-c, humanin, and SHLP peptides, with emphasis on age-related changes and therapeutic potential.
Limitations
- Most data from animal models and observational human studies
- Causality between MDP decline and aging not established
- Exogenous MDP supplementation may not replicate endogenous functions
- Limited long-term safety data for chronic MDP supplementation
- Relationship between circulating and tissue MDP levels unclear
Relevance to Content
Excellent for longevity-focused MOTS-c content. The “decline with aging” narrative parallels NAD+, CoQ10, and other longevity molecules. Positions MOTS-c within the broader mitochondrial health framework. The Cohen lab authorship provides authority. Useful for content connecting MOTS-c to the larger anti-aging/longevity conversation.
See Also
- Parent compound: MOTS-c