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Galactose-modified cytotoxic prodrugs preferentially target senescent cells because these have characteristically high expression of -galactosidase

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Notably, depletion (rather than pharmacologic inhibition) of PRMT1 significantly suppressed fibroblast proliferation, linking intracellular arginine methylation to fibrotic remodeling [90]

The two drugs synergistically promote HMOX1 expression and subsequently increase the intracellular free iron ion levels, leading to ferroptosis in hepatocellular carcinoma (HCC) cells 15