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When combined with anti-CTLA-4 therapy, this remodeling approach effectively suppressed tumor growth in CRC models rich in CAFs (75)

[25] NAD+ repletion restored NAD+ metabolic profiles, improved fat metabolism, lowered mitochondrial oxidative stress, and improved mitochondrial integrity in human cells with mutant WRN via restoring normal mitophagy

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-Synuclein aggregation nucleates through liquidliquid phase separation

Oxidative stress plays an important role in the pathogenesis of both ischemic brain damage and the response to it [2, 3]