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Mechanistically, melatonin increases the expression of mitochondrial markers (PINK1, PRKN, and LC3-II), enhances mitochondrial autophagic flux by upregulating the expression of SIRT3, and increasing the SIRT3-mediated TFAM deacetylation level at the K154 site to promote mitochondrial autophagy flux, thereby alleviating SAKI (Deng et al., 2024)

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Vergadi et al., 2017)

Q: How do GHRP half-lives affect study design