ACSL4-Mediated Ferroptosis and its Biological Functions and Potential Therapeutic Significance in Liver Diseases

As the body's main metabolic organ, the liver performs many crucial functions. Liver diseases such as hepatitis and liver cancer are chronic diseases that can seriously damage health. Currently, effective therapeutic strategies remain limited. In recent years, ferroptosis has become an emerging therapeutic target in the diagnosis and treatment of human diseases. Initially identified in tumor cells linked to neurological disorders, it has recently been acknowledged as a crucial element in the advancement of hepatic ailments. Acyl-CoA synthetase long-chain family member 4 (ACSL4) could be a target for ferroptosis driven by unsaturated fatty acid (FA). More specifically, overexpression of ACSL4 causes reactive oxygen species (ROS) and lipid peroxidation (LPO) products to accumulate, therefore aggravating the course of liver cell ferroptosis. Given that ACSL4 has a complex involvement in liver pathophysiology, its targeted control may represent a novel therapeutic approach for liver illnesses. Even so, more research is required to better understand the molecular mechanisms of ACSL4 and its clinical implications. This article will focus on elucidating the key regulatory molecular mechanisms of ACSL4 in ferroptosis and liver disease progression, aiming to highlight ACSL4 as a potential therapeutic target and provide deep insights into the molecular basis of liver pathology.