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Reversing such damage to these organelles can mitigate copper-induced apoptosis (48, 53)

Interestingly, these molecules exert pro-inflammatory effects through acetylation, oxidation, and especially induce aggregation with additional molecules (209)

J Exp Med 213:15131535

In the process of hepatocellular steatosis, one of the hallmarks of MASLD is the appearance of the UPR in hepatocytes, which can inhibit mitochondrial lipid oxidation through the UPR-induced ATF-6 pathway and promote fatty acid synthesis via the PERK, ATF-6 and IRE1 signaling pathways, which together promote intracellular lipid accumulation (67,68)