Abstract
In recent years, the prevalence of metabolic dysfunction‑associated steatotic liver disease (MASLD), which was called non-alcoholic fatty liver disease (NAFLD), has been progressively increasing in populations. The progression of MASLD encompasses a spectrum from simple steatosis to metabolic dysfunction-associated steatohepatitis (MASH), and ultimately to cirrhosis or even hepatocellular carcinoma. During the early stages of the disease, lipid accumulation and endoplasmic reticulum stress may lead to abnormalities in hepatic DNA expression, protein synthesis, and post-translational modifications (PTMs). PTMs play a crucial role in the progression of MASLD and include histone and non-histone modifications, with major types including methylation, acetylation, ubiquitination, and phosphorylation. Numerous studies indicate that within MASLD-related signaling pathways, PTMs can modulate protein activity, localization, folding, and interactions by altering their physicochemical properties. This review summarizes various significant PTMs involved in MASLD progression to elucidate the regulatory mechanisms and pathogenesis associated with the disease.