The Mechanism and Therapeutic Prospect of Autophagy in Metabolic Dysfunction-Associated Steatotic Liver Diseas

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) has become the most common chronic liver disease in the world. Metabolic dysfunction-associated steatohepatitis (MASH) is an inflammatory subtype of MASLD, which can further develop into cirrhosis and hepatocellular carcinoma. With the global prevalence of metabolic syndrome, obesity and diabetes, the prevalence of MASLD is increasing year by year, which has brought an increasingly heavy burden to the global economy. Although steady progress has been made in understanding the epidemiology and pathogenesis of the disease, it is still the slowest progress in the treatment field. At present, there is a lack of approved specific therapeutic drugs. Therefore, it is urgent to further analyze the pathogenesis of MASLD and explore new therapeutic targets. In recent years, the role of autophagy in the pathogenesis of MASLD is being extensively studied. It is mainly involved in the occurrence and progression of the disease by regulating multiple factors such as lipotoxicity, mitochondrial dysfunction, oxidative stress, insulin resistance (IR), endoplasmic reticulum stress (ERS), inflammasome activation, and intestinal flora imbalance.