ArticleCommunications biology2025
STAT1 promotes ferroptosis and inflammation in mouse hepatic ischemia-reperfusion injury.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Pathophysiological mechanisms of cell death affecting graft survival in liver transplantation.World journal of transplantation · 2026Review
- STAT1: a central hub linking ferroptosis and inflammation in hepatic ischemia-reperfusion injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- T Cell-Derived IFN-γ Activates Ferroptosis in Lacrimal Luminal Ductal Cells via JAK-STAT Signaling in Sjögren's Disease-Related Dry Eye.Investigative ophthalmology & visual science · 2026Article
- Ninjurin-1 mediates hepatic ischemia-reperfusion injury.Science advances · 2026Article
- Preconditioning with sufentanil confers protective effects in transplantation by attenuating hepatic ischemia-reperfusion injury.World journal of transplantation · 2026Review
- Vitamin B12 Alleviates Hepatic Ischemia-Reperfusion Injury with Restoration of Propanoate Metabolism and Mitochondrial Function.Journal of inflammation research · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
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Abstract
Hepatic ischemia reperfusion injury (HIRI) is a critical complication in liver surgery and transplantation, driven by excessive inflammation and hepatocellular death. Although ferroptosis is recognized as a major form of regulated cell death in HIRI, the upstream regulators of this process remain poorly defined. Here, we show that the transcription factor STAT1 plays a pivotal role in promoting ferroptosis and inflammation during HIRI. Using male mice subjected to partial hepatic ischemia followed by reperfusion, we find that STAT1 protein is significantly upregulated in liver tissues. Genetic deletion of Stat1 markedly reduces lipid peroxidation, suppresses proinflammatory cytokine expression, and improves liver histology and function. Mechanistically, STAT1 represses miR-497-5p transcription, leading to HDAC7 activation, which together promotes ferroptosis and inflammatory responses in HIRI. These results identify STAT1 as a central link between ferroptosis and inflammation in HIRI, suggesting that targeting STAT1 may offer a novel therapeutic strategy for liver protection in clinical settings.
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Registered trials
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