ArticleEMBO molecular medicine2022
A type IV Autotaxin inhibitor ameliorates acute liver injury and nonalcoholic steatohepatitis.
Article in EMBO molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- CHML regulates migration and invasion in hepatocellular carcinoma via transcriptional and metabolic reprogramming.Frontiers in oncology · 2025Article
- High intake of n-6 polyunsaturated fatty acid exacerbates non-alcoholic steatohepatitis by the involvement of multiple metabolic pathways.Frontiers in nutrition · 2025Article
- Effect of an Autotaxin Inhibitor, 2-(4-Chlorophenyl)-7-methyl-8-pentylimidazo[1,2-ACS pharmacology & translational science · 2024Article
- Marginal Maternal Zinc Deficiency Produces Liver Damage and Altered Zinc Transporter Expression in Offspring Male Rats.Biological trace element research · 2024Article
- Phosphorylation: new star of pathogenesis and treatment in steatotic liver disease.Lipids in health and disease · 2024Article
- TRIB1 regulates liver regeneration by antagonizing the NRF2-mediated antioxidant response.Cell death & disease · 2023Article
- A type IV Autotaxin inhibitor ameliorates acute liver injury and nonalcoholic steatohepatitis.EMBO molecular medicine · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The lysophosphatidic acid (LPA) signaling axis is an important but rather underexplored pathway in liver disease. LPA is predominantly produced by Autotaxin (ATX) that has gained significant attention with an impressive number of ATX inhibitors (type I-IV) reported. Here, we evaluated the therapeutic potential of a (yet unexplored) type IV inhibitor, Cpd17, in liver injury. We first confirmed the involvement of the ATX-LPA signaling axis in human and murine diseased livers. Then, we evaluated the effects of Cpd17, in comparison with the classic type I inhibitor PF8380, in vitro, where Cpd17 showed higher efficacy. Thereafter, we characterized the mechanism-of-action of both inhibitors and found that Cpd17 was more potent in inhibiting RhoA-mediated cytoskeletal remodeling, and phosphorylation of MAPK/ERK and AKT/PKB. Finally, the therapeutic potential of Cpd17 was investigated in CCl
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.