ArticleJournal of cellular and molecular medicine2022
Deficiency of Ninjurin1 attenuates LPS/D-galactosamine-induced acute liver failure by reducing TNF-α-induced apoptosis in hepatocytes.
Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- NINJ1: implications for plasma membrane rupture and disease.Biochemical Society transactions · 2026Review
- Ubc9-mediated SUMOylation of Ninj1 alleviates inflammatory responses in hepatic ischaemia/reperfusion injury.Clinical and translational medicine · 2026Article
- Regulated necrosis at the crossroads of liver inflammation and cancer development.Nature reviews. Gastroenterology & hepatology · 2026Review
- The role of NINJ1 in diseases.Cell death discovery · 2026Review
- Digging deeper into NINJ1: its multifaceted role in central nervous system diseases.Frontiers in immunology · 2026Review
- Silibinin alleviates acute liver failure by modulating AKT/GSK3β/Nrf2/GPX4 pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Pyroptosis: molecular mechanisms and roles in disease.Cell research · 2025Review
- Targeting NINJ1-mediated cell rupture to treat inflammatory diseases.Molecular medicine (Cambridge, Mass.) · 2025Review
- Advances in Understanding Lipopolysaccharide-Mediated Hepatitis: Mechanisms and Pathological Features.Current issues in molecular biology · 2025Review
- Gasdermins as evolutionarily conserved executors of inflammation and cell death.Nature cell biology · 2024Review
- NINJ1 Regulates Platelet Activation and PANoptosis in Septic Disseminated Intravascular Coagulation.International journal of molecular sciences · 2023Article
- Deficiency of Ninjurin1 attenuates LPS/D-galactosamine-induced acute liver failure by reducing TNF-α-induced apoptosis in hepatocytes.Journal of cellular and molecular medicine · 2022Article
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Nerve injury-induced protein 1 (Ninjurin1, Ninj1) is a membrane protein that mediates cell adhesion. The role of Ninj1 during inflammatory response has been widely investigated in macrophages and endothelial cells. Ninj1 is expressed in various tissues, and the liver also expresses high levels of Ninj1. Although the hepatic upregulation of Ninj1 has been reported in human hepatocellular carcinoma and septic mice, little is known of its function during the pathogenesis of liver diseases. In the present study, the role of Ninj1 in liver inflammation was explored using lipopolysaccharide (LPS)/D-galactosamine (D-gal)-induced acute liver failure (ALF) model. When treated with LPS/D-gal, conventional Ninj1 knock-out (KO) mice exhibited a mild inflammatory phenotype as compared with wild-type (WT) mice. Unexpectedly, myeloid-specific Ninj1 KO mice showed no attenuation of LPS/D-gal-induced liver injury. Whereas, Ninj1 KO primary hepatocytes were relatively insensitive to TNF-α-induced caspase activation as compared with WT primary hepatocytes. Also, Ninj1 knock-down in L929 and AML12 cells and Ninj1 KO in HepG2 cells ameliorated TNF-α-mediated apoptosis. Consistent with in vitro results, hepatocyte-specific ablation of Ninj1 in mice alleviated LPS/D-gal-induced ALF. Summarizing, our in vivo and in vitro studies show that lack of Ninj1 in hepatocytes diminishes LPS/D-gal-induced ALF by alleviating TNF-α/TNFR1-induced cell death.
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Registered trials
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 OpenQuestion graph.