ArticleJournal of molecular medicine (Berlin, Germany)2022
Receptor-interacting protein kinase-1 ablation in liver parenchymal cells promotes liver fibrosis in murine NASH without affecting other symptoms.
Article in Journal of molecular medicine (Berlin, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- TGFBI in tumors and the tumor immune microenvironment: functional roles, mechanisms, and therapeutic targeting.Frontiers in immunology · 2026Review
- Glycolysis in hepatic stellate cells coordinates fibrogenic extracellular vesicle release spatially to amplify liver fibrosis.Science advances · 2024Article
- The scaffold-dependent function of RIPK1 in experimental non-alcoholic steatohepatitis.Journal of molecular medicine (Berlin, Germany) · 2022Article
- RIPK1 in Liver Parenchymal Cells Limits Murine Hepatitis during Acute CClInternational journal of molecular sciences · 2022Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
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Abstract
Non-alcoholic steatohepatitis (NASH), a chronic liver disease that emerged in industrialized countries, can further progress into liver fibrosis, cirrhosis, and hepatocellular carcinoma. In the next decade, NASH is predicted to become the leading cause of liver transplantation, the only current interventional therapeutic option. Hepatocyte death, triggered by different death ligands, plays key role in its progression. Previously, we showed that the receptor-interacting protein kinase-1 (RIPK1) in hepatocytes exhibits a protective role in ligand-induced death. Now, to decipher the role of RIPK1 in NASH, Ripk1
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