ArticleFrontiers in endocrinology2023
Receptor-interacting protein 1 and 3 kinase activity are required for high-fat diet induced liver injury in mice.
Article in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- β-Caryophyllene Mitigates Thioacetamide-Induced Liver Fibrosis Through CB2-Mediated Suppression of Necroptosis: A Therapeutic Investigation.Pharmacology research & perspectives · 2026Article
- Suboptimal Selenium Intake Produces Sex-Specific Alterations in Metabolic Profiles in Western Diet-Fed Obese Mice.International journal of molecular sciences · 2026Article
- LSECtin attenuates hepatic Th17 expansion in a murine model of cirrhosis and signals through the LAG-3 receptor.JHEP reports : innovation in hepatology · 2025Article
- Mechanistic Elucidation ofJournal of agricultural and food chemistry · 2025Article
- The TNFR-RIPK1/RIPK3 signalling pathway mediates the effect of lanthanum on necroptosis of nerve cells.Open life sciences · 2025Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Background: The RIP1-RIP3-MLKL-mediated cell death pathway is associated with progression of non-alcohol-associated fatty liver/steatohepatitis (NAFL/NASH). Previous work identified a critical role for MLKL, the key effector regulating necroptosis, but not RIP3, in mediating high fat diet-induced liver injury in mice. RIP1 and RIP3 have active N-terminus kinase domains essential for activation of MLKL and subsequent necroptosis. However, little is known regarding domain-specific roles of RIP1/RIP3 kinase in liver diseases. Here, we hypothesized that RIP1/RIP3 kinase activity are required for the development of high fat diet-induced liver injury. Methods: Results: Both Discussion: The current data indicate that both RIP1 and RIP3 kinase activity contribute to FFC diet-induced liver injury. This effect of RIP1 and RIP3 kinase deficiency on injury is consistent with the protection of
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