Hepatocyte FoxO1 depletion exacerbates hepatic inflammation in MASH by targeting cystathionine γ-lyase - Chen, Hui-Ting; Huang, Chen; Chen, Jia-Wei; Yang, Si-Qi; Cheng, Jie-Min; Li, Yong-Qiang; Chen, Han-Qing; Zhou, Yong-Jian (Scientific reports, 2025)
Keywords: 692/4020; 692/699; Animals; Biotechnology; CTH; Cystathionine g-lyase; Cystathionine gamma-Lyase - genetics; Cystathionine gamma-Lyase - metabolism; Feeds; Forkhead Box Protein O1 - deficiency; Forkhead Box Protein O1 - genetics; Forkhead Box Protein O1 - metabolism; Forkhead protein; FoxO1; FOXO1 protein; Genes; Glucose metabolism; Hepatocyte; Hepatocytes; Hepatocytes - metabolism; Hepatocytes - pathology; Humanities and Social Sciences; Inflammation; Inflammation - metabolism; Inflammation - pathology; L-Alanine; Life sciences; Lipid metabolism; Lipopolysaccharides; Liver; Liver - metabolism; Liver - pathology; Liver diseases; Male; MASH; Metabolism; Metabolites; Methionine; Mice; Mice, Inbred C57BL; Mice, Knockout; multidisciplinary; Nutrient deficiency; Polymerase chain reaction; Proteins; Reagents; Science; Science (multidisciplinary); Therapeutic targets; Transcriptomics; Tumor Necrosis Factor-alpha - metabolism; Tumor necrosis factor-α; United States--US; China; Japan; MASH; Inflammation; Hepatocyte; CTH; FoxO1