Targeting Acyl-CoA synthetase long-chain family member 4: a potential approach for the treatment of cerebral ischemia/reperfusion injury.

Cerebral ischemia/reperfusion injury causes high rates of morbidity and death. Recent studies have shown that ferroptosis, a type of controlled cell death brought on by lipid peroxidation, worsens cerebral ischemia/reperfusion injury. Acyl-CoA synthetase long-chain family member 4 (ACSL4) has emerged as a crucial enzyme in lipid metabolism and ferroptosis in the context of ischemia/reperfusion injury, influencing neuronal cell death. Increased vulnerability to ferroptosis and worsening ischemia/reperfusion injury outcomes are linked to elevated ACSL4 levels. Comprehending the molecular processes underlying ACSL4-mediated ferroptosis may result in novel approaches to treating cerebral ischemia/reperfusion injury. The present review discusses ACSL4 as a potential target for treating cerebral ischemia/reperfusion injury, focusing on ACSL4-mediated ferroptosis and signal transduction.