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KD inhibit the activation of synthesize 3-hydroxy-3-methylglutaryl-CoA (HMG CoA) while activating HMG-CoA lyase (HMGCL), thereby promoting the production of ketone bodies and concurrently reducing the synthesis of endogenous total cholesterol (TC) [88, 89]

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This eliminates injection site variability as a factor when evaluating dose effectiveness

TREX2 degrades cytosolic DNA, repressing cGAS-STING activation, leading to less apoptosis of tumor cells and downregulated CD8 + T cell infiltration in the TME, ultimately enhancing resistance to immunoblockade therapy [17]

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MOTS-c improves mitochondrial function for improved energy use, while FTPP causes fat cell death