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Co-culture experiments showed that AMSCs can significantly reduce JNK activation (mitochondrial stress) and the expression of H2AX (DNA damage) caused by APAP toxicity and increase the expression of DDIT4 in AML12 cells and primary hepatocytes (Fig

ROS also promote fibrosis by inducing epigenetic changes such as DNA methylation, with the associated DNA hypermethylation downregulating several anti-fibrotic genes [157], thereby exacerbating the progression of intestinal fibrosis

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4g) incorporating a PD-L1 binding peptide, a self-assembly linker, and an E3 ligase ligand