Research

Longevity research is increasingly focused on restoring cellular homeostasis,  supporting extracellular-matrix renewal, mitochondrial efficiency, and oxidative-stress balance. In skin and connective tissues, the copper-binding tripeptide GHK-Cu has been shown to up-regulate regenerative gene networks and stimulate collagen and ECM remodeling, mechanisms that align with healthier tissue ageing trajectories [1].

At the metabolic level, NAD⁺ is a critical redox cofactor that fuels sirtuin and PARP activity, maintaining DNA repair and mitochondrial function. Experimental and review studies indicate that replenishing NAD⁺ pools through precursors or pathway activation improves metabolic flexibility and attenuates age-related decline across tissues [2,3].

Emerging mitochondrial-targeted peptides add a complementary dimension. MOTS-C, encoded by mitochondrial DNA, enhances glucose metabolism and exercise-like adaptations, contributing to metabolic resilience during ageing [4,5]. SS-31 (Elamipretide), which binds cardiolipin within mitochondrial membranes, has been shown to reduce oxidative damage, stabilize bioenergetics, and preserve cognitive and muscular performance in ageing models [6,7]. Collectively, these peptides illustrate how matrix regeneration, mitochondrial protection, and redox balance form key pillars of research into healthy longevity.

References

1. Pickart L, Margolina A. Regenerative and protective actions of the GHK-Cu peptide in the light of new gene data.Int J Mol Sci. 2018;19(7):1987. PMID: 29986520 (Open-access PMCID available) PubMed+1

2. Verdin E. NAD⁺ in aging, metabolism, and neurodegeneration. Science. 2015;350(6265):1208–1213. PMID:26785480 PubMed

3. Yoshino J, Baur JA, Imai S-i. NAD⁺ intermediates: the biology and therapeutic potential of NMN and NR. Cell Metab. 2018;27(3):513–528. PMID: 29249689 (Epub late-2017; in 2018 issue) PubMed

4. Lee C, Zeng J, Drew BG, et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity/insulin resistance. Cell Metab. 2015;21(3):443–454. PMID: 25738459 PubMed

5. Kim KH, Son JM, Benayoun BA, Lee C. The mitochondrial-encoded peptide MOTS-c translocates to the nucleus to regulate gene expression with metabolic stress. Cell Metab. 2018;28(3):516–524.e7. PMID: 29983246PubMed

6. Tarantini S, et al. Treatment with the mitochondrial-targeted antioxidant peptide SS-31 rescues neurovascular coupling and cognition in aged mice. Aging Cell. 2018;17(3):e12740. PMID: 29405550 (PMCID available) PubMed+1

7. Campbell MD, Duan J, Samuelson AT, et al. Improving mitochondrial function with SS-31 reverses age-related redox stress and improves exercise tolerance in aged mice. Free Radic Biol Med. 2019;134:268–281. PMID:30597195