ArticleCell death & disease2014
TRAF1 is a key mediator for hepatic ischemia/reperfusion injury.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
The trial behind it
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Who cites it
22 citing papers in PubMed.
- Helicobacter pylori VacA modulates TRAF1-mediated 4-1BB/NF-kappaB axis to induce host apoptosis and chronic inflammatory damage.Molecular medicine (Cambridge, Mass.) · 2025Article
- Electroacupuncture Attenuates Hepatic Ischemia-Reperfusion Injury by Modulating the Esr1/TAK1-JNK/p38 Signaling Pathway in Rats.Mediators of inflammation · 2025Article
- Upregulation of fatty acid synthesis genes in the livers of adolescent female rats caused by inhalation exposure to PCB52 (2,2',5,5'-Tetrachlorobiphenyl).Environmental toxicology and pharmacology · 2024Article
- TRAF1 from a Structural Perspective.Biomolecules · 2024Review
- Chinese herbal formula in the treatment of metabolic dysfunction-associated steatotic liver disease: current evidence and practice.Frontiers in medicine · 2024Review
- Elabela inhibits TRAF1/NF-κB induced oxidative DNA damage to promote diabetic foot ulcer wound healing.iScience · 2023Article
- CD40/TRAF1 decreases synovial cell apoptosis in patients with rheumatoid arthritis through JNK/NF-κB pathway.Journal of bone and mineral metabolism · 2022Article
- The Role of Tumor Necrosis Factor Associated Factors (TRAFs) in Vascular Inflammation and Atherosclerosis.Frontiers in cardiovascular medicine · 2022Review
- Identification of the Key Regulators of Spina Bifida Through Graph-Theoretical Approach.Frontiers in genetics · 2021Article
- Safety and efficacy ofHeliyon · 2020Article
- Roles of TRAFs in Ischemia-Reperfusion Injury.Frontiers in cell and developmental biology · 2020Review
- TRAF1 Exacerbates Myocardial Ischemia Reperfusion Injury via ASK1-JNK/p38 Signaling.Journal of the American Heart Association · 2019Article
- miR-214 Down-Regulation Promoted Hypoxia/Reoxygenation-Induced Hepatocyte Apoptosis Through TRAF1/ASK1/JNK Pathway.Digestive diseases and sciences · 2019Article
- TRAF2 protects against cerebral ischemia-induced brain injury by suppressing necroptosis.Cell death & disease · 2019Article
- Insights into the Epidemiology, Pathogenesis, and Therapeutics of Nonalcoholic Fatty Liver Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2019Review
- Targeting F-Box Protein Fbxo3 Attenuates Lung Injury Induced by Ischemia-Reperfusion in Rats.Frontiers in pharmacology · 2019Article
- TRAF molecules in inflammation and inflammatory diseases.Current pharmacology reports · 2018Article
- The deubiquitinating enzyme cylindromatosis mitigates nonalcoholic steatohepatitis.Nature medicine · 2018Article
- Ischemia/Reperfusion.Comprehensive Physiology · 2016Review
- Innate Immune Regulations and Liver Ischemia-Reperfusion Injury.Transplantation · 2016Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor necrosis factor receptor-associated factor 1 (TRAF1), an adapter in signal transduction, is involved in immunity and in apoptotic processes in various cell types. However, little is known about its function and the molecular mechanism of its activation during liver injury. This study tested the hypothesis that TRAF1 is a mediator of cell injury after hepatic ischemia/reperfusion injury (I/R). In a mouse hepatic I/R injury model, we found that TRAF1 expression was highly induced. TRAF1 deficiency was liver protective, whereas sustained TRAF1 overexpression aggravated liver injury in response to hepatic I/R injury. Mechanistic studies demonstrated that a deficiency of TRAF1 in cultured hepatocytes led to the inhibition of NF-κB-mediated inflammatory responses, suppression of the ASK/JNK pro-death pathway and promotion of cellular regeneration capacity. In contrast, the converse occurred in hepatocyte-specific TRAF1 transgenic mice. TRAF1 activated the ASK1/JNK pathway and promoted hepatic injury. Our study demonstrates that TRAF1 is a crucial early mediator of hepatic I/R injury and suggests that TRAF1 may be a potential gene therapy target for the treatment of liver injury.
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