Autophagy, Mitophagy, and MOTS-c #peptidemedicine #praxispeptideinstitute

Autophagy is not just cellular cleanup. It is a feedback system. Mitophagy removes damaged mitochondria before they create a loop of oxidative stress, inflammation, low energy, and accelerated aging biology. And this is where MOTS-c becomes fascinating: a mitochondrial-derived peptide that may help coordinate stress adaptation, AMPK-linked signaling, metabolism, inflammation, and mitochondrial resilience. Not hype. Signal biology. praxispeptideinstitute.com #Autophagy #Mitophagy #MOTSc #Mitochondria #PeptideMedicine #LongevityScience #CellularHealth #AMPK #MitochondrialHealth #Inflammation #MetabolicHealth #Bioenergetics #HealthOptimization #PraxisEvidenceCheck #EvidenceBasedHealth Shan, W., Liu, Y., Tang, R., Li, H., Yang, H., & Lin, L. (2026). Targeting mitochondrial autophagy for anti-aging. Cell Death Discovery, 12, Article 78. https://doi.org/10.1038/s41420-025-02... This is the main mitophagy/autophagy-aging review. Wan, W., Zhang, L., Lin, Y., Rao, X., Wang, X., Hua, F., & Ying, J. (2023). Mitochondria-derived peptide MOTS-c: Effects and mechanisms related to stress, metabolism and aging. Journal of Translational Medicine, 21, Article 36. https://doi.org/10.1186/s12967-023-03... This is the main MOTS-c review covering stress response, AMPK signaling, metabolism, inflammation, exercise, and aging. Lee, C., Zeng, J., Drew, B. G., Sallam, T., Martin-Montalvo, A., Wan, J., Kim, S.-J., Mehta, H., Hevener, A. L., de Cabo, R., & Cohen, P. (2015). The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metabolism, 21(3), 443–454. https://doi.org/10.1016/j.cmet.2015.0... This is the foundational MOTS-c discovery/metabolic homeostasis paper. Kim, K. H., Son, J. M., Benayoun, B. A., & Lee, C. (2018). The mitochondrial-encoded peptide MOTS-c translocates to the nucleus to regulate nuclear gene expression in response to metabolic stress. Cell Metabolism, 28(3), 516–524.e7. https://doi.org/10.1016/j.cmet.2018.0... This is the key paper for the “mitochondrial-to-nuclear feedback signal” concept.