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Lipotoxicity-Induced STING1 Activation Stimulates MTORC1 and Restricts Hepatic Lipophagy

[Autophagy] It is still unknown how hepatic inflammation regulates lipid metabolism in hepatocytes. Scientists found that PA treatment or direct stimulation of STING1 promoted, whereas STING1 deficiency impaired, MTORC1 activation, suggesting that STING1 was involved in PA-induced MTORC1 activation.

Critical Role for Hepatocyte-Specific eNOS in NAFLD and NASH

[Diabetes] Scientists showed genetic deletion and viral knockdown of hepatocyte-specific endothelial nitric oxide synthase (eNOS) exacerbated hepatic steatosis and inflammation, decreased hepatic mitochondrial fatty acid oxidation and respiration, increased mitochondrial H2O2 emission, and impaired the hepatic mitophagic response.

89bio Completed Target Enrollment in Histology Cohort to Evaluate BIO89-100 for the Treatment of NASH

[89bio, Inc.] 89bio, Inc announced that it has completed target enrollment of 20 patients in the paired-biopsy, open-label histology cohort in biopsy-confirmed fibrosis stage F2 – F3 NASH patients.

Addressing the Liver Progenitor Cell Response and Hepatic Oxidative Stress in Experimental Non-Alcoholic Fatty Liver Disease/Non-Alcoholic Steatohepatitis Using Amniotic Epithelial Cells

[Stem Cell Research & Therapy] Scientists examined the effect human amniotic epithelial cells have on the liver progenitor cell response and hepatic oxidative stress in an experimental model of non-alcoholic steatohepatitis.

Histone Deacetylase Inhibitor Givinostat Attenuates Nonalcoholic Steatohepatitis and Liver Fibrosis

[Acta Pharmacologica Sinica] Researchers evaluated the therapeutic potential of givinostat, a histone deacetylase inhibitor, in the treatment of nonalcoholic steatohepatitis in vivo and in vitro.

Pathophysiological Communication between Hepatocytes and Non-Parenchymal Cells in Liver Injury from NAFLD to Liver Fibrosis

[Advanced Drug Delivery Reviews] Reseachers overview recent findings from human study and animal models on the pathophysiological communication among hepatocytes, Kupffer cells, hepatic stellate cells and liver sinusoidal endothelial cells during the disease development.

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