Activated cGAS-STING signaling promotes malignancy in metabolic dysfunction-associated fatty liver disease via mitochondrial DNA and immune cell dysfunction

Figure 5 Dynamic alteration of cell clustering in the liver. A: Clustering of liver cells in control rats; the numbers of cells in liver cell subpopulations; B: Dynamic changes in cell subpopulations in different livers (n = 5; that is, normal control, metabolic dysfunction-associated fatty liver disease, metabolic dysfunction-associated steato-hepatitis, liver cirrhosis and hepatocellular carcinoma) during malignant progression. The following cell types were identified: Hepatocytes (0, 20, 23, 24, 27); B cells (2, 25, 28); endothelial cells (3, 1; natural killer cells (6, 10, 13); T cells, monocytes, macrophages (7, 9, 12, 15); dendritic cells (8); neutrophils (11); epithelial cells (19); red blood cells (21); plasma cells (26); hepatocytes (29); and dendritic cells (33). Unidentified cells (1, 4, 5, 14, 16, 18, 22, 30, 31, 32). t-SNE-1: T-distributed stochastic neighbor embedding-1; t-SNE-2: T-distributed stochastic neighbor embedding-2; NC: Normal control; MAFLD: Metabolic dysfunction-associated fatty liver disease; MASH: Metabolic dysfunction-associated steatohepatitis; LC: Liver cirrhosis; HCC: Hepatocellular carcinoma.