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In addition, pharmacological interventions of FAO had obvious effects on IR injury, i.e., the activation of CPT1-dependent FAO by leptin significantly attenuated IR-induced injury, which is manifested by reduced hepatic enzyme level, hepatic injury score, hepatocyte apoptosis, and mitochondrial damage, while the inhibition of CPT1 by etomoxir imparted negative effects

doi:10.3389/fnins.2022.874750

NOX enzymes are activated by diverse mediators, including PDGF [78], angiotensin II [79], leptin [80, 81], alcohol [82], and phagocytosis of apoptotic hepatocyte bodies [83]

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