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Furthermore, nintedanib inhibited UUO-elicited renal proinflammatory cytokine expression and macrophage infiltration [222]

Cell 82 , 447462 (2022)

This interaction highlights the coordinated regulation where ATF4 and ATF3 binding to these elements modulates CHAC1 expression, linking it to the cellular stress response pathways (Romanoski et al., 2011)

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APAP can aggravate oxidative stress and induce ferroptosis, a mode of cell death mediated by lipid peroxidation and cellular free iron when protective mechanisms such as glutathione peroxidase activity have been compromised (Figure 10F)