Telomerase activation, AMPK signaling, and NAD+ metabolism
Longevity research peptides target fundamental cellular aging mechanisms including telomere maintenance, mitochondrial function, and metabolic cofactor homeostasis.
Epithalon (Ala-Glu-Asp-Gly) activates human telomerase reverse transcriptase (hTERT) expression, the catalytic subunit of telomerase. This enzyme adds TTAGGG repeats to chromosome ends, counteracting replicative senescence. Additionally, Epithalon modulates melatonin secretion through pinealocyte stimulation and may upregulate antioxidant enzymes SOD and GPx.
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MOTS-c is encoded within the 12S rRNA gene of mitochondrial DNA, representing a novel class of retrograde mitochondrial signaling molecules. It activates AMPK, the master metabolic regulator, promoting GLUT4 translocation for glucose uptake. Under metabolic stress, MOTS-c translocates to the nucleus where it regulates gene expression involved in the folate-methionine cycle and purine biosynthesis.
NAD+ is a substrate for sirtuins (SIRT1-7), PARPs, and CD38. Age-related NAD+ decline is associated with mitochondrial dysfunction, impaired DNA repair, and cellular senescence. Research examines whether NAD+ supplementation can restore the NAD+/NADH ratio and reactivate sirtuin-dependent pathways.
These compounds address aging at different levels: Epithalon at the chromosomal level (telomeres), MOTS-c at the organelle level (mitochondria), and NAD+ at the enzymatic/metabolic level (sirtuins, PARPs). Together they form the Longevity Research Stack for comprehensive aging pathway investigation.
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