In the context of liver fibrosis, Fan et al
By inhibiting the folate cycle and de novo purine synthesis, MOTS-c triggers an AMPK-driven shift that encourages the body to burn fuel rather than store it
The effects persisted beyond the peptide's pharmacokinetic half-life, supporting the "trigger" hypothesis (PMID 514474)
This restoration of metabolic cofactor availability enables enhanced function of NAD+-dependent enzymes including sirtuins, poly(ADP-ribose) polymerases, and various deacetylases that regulate cellular metabolism, stress responses, and aging processes

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