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hepatic cells

Roles of IκB Kinases and TANK-Binding Kinase 1 in Hepatic Lipid Metabolism and Nonalcoholic Fatty Liver Disease

[Experimental and Molecular Medicine] The authors review the biochemical steps of hepatic lipid metabolism, dysregulated lipid metabolism in obesity and nonalcoholic fatty liver disease (NAFLD), and the roles of IκB kinase complexes and TANK-binding kinase 1 in obesity and NAFLD.

Initiation of Hepatic Stellate Cell Activation Extends into Chronic Liver Disease

[Cell Death & Disease] Scientists identified transcriptional programs of initiating and activated hepatic stellate cells by RNA sequencing, using in vitro and in vivo mouse models of fibrosis.

Sorafenib Attenuates Liver Fibrosis by Triggering Hepatic Stellate Cell Ferroptosis via HIF-1α/SLC7A11 Pathway

[Cell Proliferation] Scientists investigate the functional role of hepatic stellate cell ferroptosis in the anti-fibrotic effect of sorafenib and found that sorafenib attenuated liver injury and extracellular matrix accumulation in CCl4-induced fibrotic livers, accompanied by reduction of SLC7A11 and GPX4 proteins.

Concurrent Disruption of Ras/MAPK and NF-κB Pathways Induces Circadian Deregulation and Hepatocarcinogenesis

[Molecular Cancer Research] Investigators showed that an unanticipated severe tumor phenotype was contributed collectively by severe cholestasis, metabolic changes, upregulated cell cycle progression and disruption of circadian rhythm in mutant hepatocytes.

Liver Ischaemia–Reperfusion Injury: A New Understanding of the Role of Innate Immunity

[Nature Reviews Gastroenterology & Hepatology] Scientists summarize the role of macrophages, platelets and neutrophils in liver ischaemia–reperfusion injury (LIRI), highlight unanswered questions, and discuss prospects for innovative therapeutic regimens against LIRI in transplant recipients.

Pseudogene RPL32P3 Regulates the Blood–Tumor Barrier Permeability via the YBX2/HNF4G Axis

[Cell Death Discovery] Researchers identified that ribosomal protein L32 pseudogene 3 (RPL32P3) was highly expressed in glioma-exposed endothelial cells. Knockdown of RPL32P3 decreased the expression of tight junction-related proteins and increased blood–tumor barrier permeability.

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