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References Cell Metabolism (2015) The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance (Lee C, Zeng J, Drew BG, et al.) Journal of Translational Medicine (2023) Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging (Wan W, Zhang L, Lin Y, et al.) Journal of Molecular Medicine (2019) MOTS-c peptide regulates adipose homeostasis to prevent ovariectomy-induced metabolic dysfunction (Lu H, Wei M, Zhai Y, et al.) Nature Communications (2021) MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis (Reynolds JC, Lai RW, Woodhead JST, et al.) Frontiers in Physiology (2023) Role of MOTS-c in the regulation of bone metabolism (Yi X, Hu G, Yang Y, et al.) International Journal of Molecular Sciences (2022) MOTS-c, the Most Recent Mitochondrial Derived Peptide in Human Aging and Age-Related Diseases (Mohtashami Z, Singh MK, Salimiaghdam N, et al.) Cognitive Vitality Reports (2021) MOTS-c (Cognitive Vitality Profile) Alzheimer's Drug Discovery Foundation (ADDF) USADA Spirit of Sport (2023) What is the MOTS-c peptide

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Nevertheless, different hypotheses were suggested to explain it

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123 CD38 downregulates NAD + by converting NAD + to cyclic-ADP riboside, mobilizing intracellular or extracellular Ca+

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Biosci Rep 17:293302, PMID: 9337484 Sato T, Machida T, Takahashi S, Iyama S, Sato Y, Kuribayashi K, Takada K, Oku T, Kawano Y, Okamoto T, Takimoto R, Matsunaga T, Takayama T, Takahashi M, Kato J, Niitsu Y (2004) Fas-mediated apoptosome formation is dependent on reactive oxygen species derived from mitochondrial permeability transition in Jurkat cells

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