Metabolic dysfunction associated fatty liver disease (MAFLD): A review on mechanistic pathways, pathophysiology, and management

Background: Metabolic dysfunction associated fatty liver disease (MAFLD) is a condition in which excess fat accumulates in the liver, without alcohol being a contributing factor. MAFLD can progress to non-alcoholic steatohepatitis (NASH), which can lead to liver cirrhosis and liver failure. Metabolic dysfunction associated fatty liver disease is also regarded as a stand-alone cardiovascular diseases' risk factor. Objective: In this review, we summarized pathophysiology, mechanistic pathways, symptoms, diagnosis, pharmacological and traditional therapeutic interventions currently being developed for treatment of MAFLD. Methods: A literature search on various data base viz Medline, PubMed, Embase, and Scopus was done using various keywords like MAFLD, NAFLD, steatosis, steatohepatitis, fibrosis, cirrhosis, adiponectin, inflammation, Result: It has been proposed that the development of MFALD is a two-step process based on this body of evidence. The hepatic deposition of fat, which will worsen insulin resistance, is the initial stage of this process. The second phase of this process consists of alterations in the extracellular matrix, energy homeostasis, cytokine injury, hyperinsulinemia, hepatic iron and/or lipid peroxidation, and oxidation of fatty acids in the liver as a result of various factors. Lifestyle modifications play a central role in managing MAFLD, and early intervention can prevent the progression of the disease to more severe forms, such as nonalcoholic steatohepatitis (NASH) or cirrhosis. Conclusion: The exact cause of MAFLD is not fully understood, but it is believed to be related to several factors. The pathogenesis of MAFLD has been shown to be profoundly influenced by inflammation and insulin resistance. The primary source of liver damage is the buildup of fat, which is followed by inflammation. A complicated relationship between adipokines and liver disease appears to be critical in the development of MAFLD. Present review aimed to explored pathophysiology of MAFLD and the development of strategies for its therapy.