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MOTS-c activates AMPK to shift cellular metabolism toward fat oxidation and improve insulin sensitivity, while 5-Amino-1MQ inhibits NNMT to preserve NAD+ availability and enhance mitochondrial function

This mechanism does not broadly stimulate cell death but instead targets a survival dependency characteristic of senescent cells

Heme mediates derepression of Maf recognition element through direct binding to transcription repressor Bach1

The activation of endothelial cells in association with the fibroblasts may lead to a strengthened skin barrier and increased skin elasticity, as well as potential acceleration in tissue repair