ArticleCell death discovery2025
Insulin-induced gene 2 alleviates ischemia-reperfusion injury in steatotic liver by inhibiting GPX4-dependent ferroptosis.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Tacrolimus (FK506) Attenuates Hepatic Ischemia-Reperfusion Injury via Oxidative Glutathione Metabolism and Suppression of Lipoxygenase-Mediated Cell Death.Antioxidants (Basel, Switzerland) · 2026Article
- The Mechanism of G Protein-Coupled Receptor Regulation of Ferroptosis in Hepatic Ischemia-Reperfusion Injury.International journal of molecular sciences · 2026Review
- METTL16 antagonizes astaxanthin-induced ferroptosis in colorectal cancer cells.Translational cancer research · 2026Article
- Metal-Organic Framework Nanoplatform Synergizes Fenton-Driven Ferroptosis and Photodynamic Apoptosis for Enhanced Hepatocellular Carcinoma Therapy.International journal of nanomedicine · 2026Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Hepatic steatosis significantly elevates the vulnerability of the graft to ischemia-reperfusion (I/R) injury during liver transplantation (LT). We investigated the protective role of insulin-induced gene 2 (Insig2) in steatotic liver's I/R injury and underlying mechanisms. Employing mouse model with Insig2 knock-out or hepatocyte-specific overexpression and high-fat diets to induce steatosis, we subjected these mice to hepatic I/R injury. The primary hepatocytes isolated from steatotic liver were used in in vitro hypoxia/reoxygenation (H/R) experiment. Our integrated in vivo and in vitro approach uncovered that Insig2 deficiency exacerbated steatotic liver's damage following hepatic I/R injury, whereas its overexpression offers protection. Mechanically, integrative analysis of transcriptome, proteome, and metabolome found that Insig2 deficiency disturbed lipid metabolism and oxidative stress homeostasis, particularly inhibiting GPX4 expression to induce ferroptosis. Furthermore, chemical inhibition of ferroptosis reversed the deleterious effect of Insig2 deficiency; whereas the protective influence of Insig2 overexpression was negated by the target inhibition of GPX4, leading to an exacerbation of hepatic I/R damage. These insights underscored the potential of the Insig2-GPX4 axis as a therapeutic target, presenting a novel avenue for enhancing the resilience of steatotic liver grafts against I/R injury.
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Registered trials
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