This review by M. Longo et al. (IRCCS – Università degli Studi di Milano, Italy) discusses how mitochondrial defects may be translated into causative explanations of NAFLD-driven hepatocellular carcinoma.
Acting as central metabolic hubs, the mitochondria rapidly adapt to different metabolic alterations to meet the biogenetic demands of the cell, also termed mitochondrial plasticity. Mitochondrial failure promotes hepatocellular damage and release signals which trigger inflammation and fibrosis. In this adverse microenvironment, hepatocytes select anti-apoptotic programs and mutations that may allow survival and proliferation.