# References — Longevity & Cellular Health Research Literature — AgeDefy Peptide

> The aggregated citation list for the AgeDefy Peptide longevity digest: peer-reviewed sources on NAD+, NMN, NR, and MOTS-c, with DOIs and PubMed links.

Every source cited across the NAD+ and MOTS-c pages and the comparison, gathered in one place.

## References

The list below aggregates the cited literature across both molecules on this desk — NAD+ and MOTS-c. Each entry gives authors, title, journal and year, with a DOI and a PubMed link where available; a single citation is listed once and referred to by its number throughout the site. Where a source is a review or commentary, the review itself is cited, not the primary studies it summarizes.

## References

[1] Vinten KT, Trętowicz MM, Coskun E, van Weeghel M, Cantó C, Zapata-Pérez R, Janssens GE, Houtkooper RH. NAD(+) precursor supplementation in human ageing: clinical evidence and challenges. Nat Metab. 2025;7:1974-1990. https://pubmed.ncbi.nlm.nih.gov/41083806/
[2] Yi L, Maier AB, Tao R, Lin Z, Vaidya A, Pendse S, Thasma S, Andhalkar N, Avhad G, Kumbhar V. The efficacy and safety of β-nicotinamide mononucleotide (NMN) supplementation in healthy middle-aged adults: a randomized, multicenter, double-blind, placebo-controlled, parallel-group, dose-dependent clinical trial. GeroScience 2023. 2023;45:29-43. https://pubmed.ncbi.nlm.nih.gov/36482258/
[3] Yoshino M, Yoshino J, Kayser BD, Patti GJ, Franczyk MP, Mills KF, Sindelar M, Pietka T, Patterson BW, Imai SI, Klein S. Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. Science. 2021;372:1224-1229. https://pubmed.ncbi.nlm.nih.gov/33888596/
[4] Covarrubias AJ, et al. NAD+ metabolism and its roles in cellular processes during ageing. Nat Rev Mol Cell Biol. 2021. https://pubmed.ncbi.nlm.nih.gov/33353981/
[5] Conze D, Brenner C, Kruger CL. Safety and Metabolism of Long-term Administration of NIAGEN (Nicotinamide Riboside Chloride) in a Randomized, Double-Blind, Placebo-controlled Clinical Trial of Healthy Overweight Adults. Sci Rep. 2019;9:9772. https://pubmed.ncbi.nlm.nih.gov/31278280/
[6] Camacho-Pereira J, Tarragó MG, Chini CCS, Nin V, Escande C, Warner GM, Puranik AS, Schoon RA, Reid JM, Galina A, Chini EN. CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism. Cell Metab. 2016;23:1127-1139. https://pubmed.ncbi.nlm.nih.gov/27304511/
[7] Koay YC, McIntosh B, Ng YH, et al. The Heart Has Intrinsic Ketogenic Capacity that Mediates NAD(+) Therapy in HFpEF. Circulation Research. 2025;136:1113-1130. https://pubmed.ncbi.nlm.nih.gov/40211954/
[8] Kumagai H, Kim SJ, Miller B, et al. MOTS-c modulates skeletal muscle function by directly binding and activating CK2. iScience. 2024;27(11):111212. https://pubmed.ncbi.nlm.nih.gov/39559755/
[9] Bolignano D, Greco M, Presta P, Duni A, et al. The Mitochondrial-Derived Peptide MOTS-c May Refine Mortality and Cardiovascular Risk Prediction in Chronic Hemodialysis Patients: A Multicenter Cohort Study. Blood Purification. 2024;53(10):824-837. https://pubmed.ncbi.nlm.nih.gov/39111290/
[10] Wan W, Zhang L, Lin Y, Rao X, Wang X, Hua F, Ying J. Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging. Journal of Translational Medicine. 2023;21(1):36. https://pubmed.ncbi.nlm.nih.gov/36670507/
[11] Reynolds JC, Lai RW, Woodhead JST, Joly JH, Mitchell CJ, Cameron-Smith D, Lu R, Cohen P, Graham NA, Benayoun BA, Merry TL, Lee C. MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nature Communications. 2021;12(1):470. https://pubmed.ncbi.nlm.nih.gov/33473109/
[12] Kim KH, Son JM, Benayoun BA, Lee C. The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress. Cell Metabolism. 2018;28(3):516-524.e7. https://pubmed.ncbi.nlm.nih.gov/29983246/

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A calm literature desk for cellular aging research — citations and context, not prescriptions and not products.