The prevalence of non-alcoholic fatty liver disease (NAFLD) is growing in parallel with that of metabolic diseases. NAFLD and metabolic syndrome, which exacerbates the risk of developing type 2 diabetes, have been shown to be heavily interlinked. Despite recent findings regarding NAFLD’s metabolic basis, its molecular basis remains unclear. Clarification of NAFLD’s molecular characteristics is crucial to developing pharmacologic therapies for its treatment before it progresses into non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma.
This article aims to investigate the molecular mechanisms and novel therapeutic strategies for NAFLD.
Dietary interventions and physical exercise are invaluable to the prevention of both metabolic disease and NAFLD. Newly discovered molecules associated with NAFLD’s pathogenesis include peroxisome proliferator-activated receptors (PPARs), adenosine monophosphate-activated protein kinase (AMPK), and c-Jun N-terminal kinase (JNK). While the development of pharmacologic therapies targeting these molecules is already underway, using these therapies in combination with lifestyle modifications may be the most effective strategy for treating NAFLD.
Furthermore, non-invasive tools to effectively stage the progression of NAFLD are urgently needed. Future research into the development of such tools should consider investigating extracellular biomarkers, which include circulating nucleic acid fragments and plasma exosomes.