LIX1L aggravates MASH-HCC progression by reprogramming of hepatic metabolism and microenvironment via CD36 - Leng, Yingrong; Zhang, Yanqiu; Cheng, Yang; Ye, Shengtao; Zheng, Ying; He, Mengmeng; Wu, Enyi; Kong, Lingyi; Zhang, Hao (Pharmacological research, 2025)
Keywords: Adipose expansion; Animals; Carcinoma, Hepatocellular - genetics; Carcinoma, Hepatocellular - metabolism; Carcinoma, Hepatocellular - pathology; CD36 Antigens - genetics; CD36 Antigens - metabolism; Disease Progression; Hepatocellular carcinoma; Humans; Lipid Metabolism; Liver - metabolism; Liver - pathology; Liver microenvironment; Liver Neoplasms - genetics; Liver Neoplasms - metabolism; Liver Neoplasms - pathology; Male; MASH; MASLD; Mice; Mice, Inbred C57BL; Mice, Knockout; Non-alcoholic Fatty Liver Disease - genetics; Non-alcoholic Fatty Liver Disease - metabolism; Non-alcoholic Fatty Liver Disease - pathology; PARylation; Poly (ADP-Ribose) Polymerase-1 - genetics; Poly (ADP-Ribose) Polymerase-1 - metabolism; RNA decay; Tumor Microenvironment; RNA decay; Hepatocellular carcinoma; MASH; Liver microenvironment; MASLD; Adipose expansion; PARylation