Hepatic stellate cells-specific LOXL1 deficiency abrogates hepatic inflammation, fibrosis, and corrects lipid metabolic abnormalities in non-obese NASH mice

• Published in: Hepatology international Vol. 15; no. 5; pp. 1122 - 1135
• Main Authors: Yang, Aiting, Yan, Xuzhen, Fan, Xu, Shi, Yiwen, Huang, Tao, Li, Weiyu, Chen, Wei, Jia, Jidong, You, Hong
• Format: Journal Article
• Language: English
• Published: New Delhi Springer India 01.10.2021; Springer Nature B.V
• Subjects: Abnormalities; Adipose tissue; Amino Acid Oxidoreductases - genetics; Amino acids; Animal models; Animals; Biopsy; Choline; Colorectal Surgery; Crosslinking; Diet; Disease Models, Animal; Extracellular matrix; Fatty liver; Fibrosis; Gene expression; Hepatic Stellate Cells - pathology; Hepatology; Humans; Inflammation; Inflammation - pathology; Leptin; Lipids; Lipogenesis; Liver; Liver - pathology; Liver Cirrhosis - pathology; Liver diseases; Lysyl oxidase; Medicine; Medicine & Public Health; Metabolic disorders; Metabolism; Mice; Mice, Inbred C57BL; Non-alcoholic Fatty Liver Disease - genetics; Non-alcoholic Fatty Liver Disease - pathology; Nutrient deficiency; Obesity; Original Article; Pathogenesis; Steatosis; Stellate cells; Surgery; NAFLD; Leptin; Liver fibrosis; Hepatic stellate cell; Lipid metabolism; Crosslink; ECM; LOXL1; Non-obese NASH; CDAA

Background and aims Lysyl oxidase-like-1 (LOXL1), a vital cross-linking enzyme in extracellular matrix (ECM) maintenance, promotes fibrosis via enhancement of ECM stability. However, the potential role of LOXL1 in the pathogenesis of nonalcoholic steatohepatitis (NASH) has not been previously studie...