Carnitine palmitoyltransferase-II inactivity promotes malignant progression of metabolic dysfunction-associated fatty liver disease via liver cancer stem cell activation

Figure 5 Validation of liver cancer stem cell activation in human metabolic dysfunction-associated fatty liver disease. A: Blood monocytes and CD44+ cells in healthy individuals; B: Blood monocytes and CD44+ cells from hepatocellular carcinoma (HCC) patients; C: Blood monocytes and CD24+ cells in healthy individuals; D: Blood monocytes and CD24+ cells in HCC patients; E: Average number of CD44+ cells in the blood of metabolic dysfunction-associated fatty liver disease (MAFLD) or HCC patients; F: Average number of CD24+ blood cells in MAFLD and HCC patients; G: A possible mechanism of hepatic carnitine palmitoyl transferase-II inactivity in MAFLD-related hepatocarcinogenesis involves the activation of LCSCs. ^bP < 0.01, compared with the normal control; LCSC: Liver cancer stem cell; MAFLD: Metabolic dysfunction-associated fatty liver disease; HFD: High-fat diet; NC: Normal control.