Metabolic dysfunction-associated fatty liver disease (MAFLD) progresses to metabolic dysfunction-associated steatohepatitis (MASH) due to mitochondrial homeostasis imbalance and dysfunction in hepatocytes caused by various factors such as lipotoxicity and inflammatory infiltration. Recent studies have confirmed that mitochondrial injury is closely associated with chronic inflammation, with extracellular vesicle (EV) acting as a key mediator linking the two processes. This article systematically reviews the molecular mechanisms of hepatocyte mitochondrial dysfunction in MAFLD/MASH, highlights the regulatory role of hepatocyte-derived EV in intrahepatic inflammation, and discusses the potential application prospects of mitochondria-targeted therapies and intercellular communication interventions in MAFLD/MASH, in order to provide a theoretical basis for developing novel therapeutic strategies for these diseases.