ArticleRedox report : communications in free radical research2025
HIF1A/BNIP3 pathway affects ferroptosis in sepsis-induced cardiomyopathy through binding to BCL-2.
Article in Redox report : communications in free radical research, 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.
- Endogenous H₂S promotes HSPA8 sulfhydration to downregulate HIF1α and prevent ferroptosis in septic myocardial injury.Redox report : communications in free radical research · 2026Article
- Astragaloside IV Reduces Sorafenib-Induced Cardiotoxicity by Inhibiting Apoptosis Through the STAT3/HIF-1α/Bcl-2 Signaling Pathway.International journal of molecular sciences · 2026Article
- Ferroptosis in Septic Cardiomyopathy Is Alleviated by Ondansetron: The Critical Role of the HTR3A-ATF3 Axis in Mitochondrial and Oxidative Homeostasis.Biomedicines · 2026Article
- Organelle homeostasis disruption: A driving force in the progression of cardiomyopathy (Review).Experimental and therapeutic medicine · 2026Review
- Inhibition of iron overload and ferroptosis attenuates sepsis-induced myocardial injury in mice through STAT3/Lcn2 pathway.Journal of cardiothoracic surgery · 2026Article
- Fundamental mechanism of ferroptosis: Three unanswered questions.Ferroptosis and oxidative stress · 2026Article
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Authors and funding
7 authors.
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Abstract
backgroundSepsis-induced cardiomyopathy (SIC) involves ferroptosis, an iron-dependent cell death. Hypoxia-inducible factor-1α (HIF-1α) regulates autophagy and apoptosis, but its role in ferroptosis remains unclear. This study investigates the interaction between the HIF1A/BNIP3 signaling pathway and the ferroptosis axis, SLC7A11/GPX4, in septic myocardial injury.
methodsA rat model of septic myocardial injury was created via cecal ligation and puncture (CLP), with an in vitro model using lipopolysaccharide (LPS)-treated H9c2 cardiomyocytes. Groups: sham, CLP, CLP + solvent, CLP + HIF1A inhibitor (LW6), CLP + ferroptosis inhibitor (Fer-1), and CLP + LW6 + Fer-1. Cardiac function, histopathological changes, and biomarkers (myocardial injury/inflammation/ferroptosis) were measured. In vitro, H9c2 cells were treated with LPS, LW6, or fenbendazole (FZ) and transfected with BNIP3 shRNA. Various assays were used to evaluate cell viability, ROS levels, and protein interactions.
results(1) HIF1A/BNIP3 activation aggravated septic myocardial injury and ferroptosis; inhibition reversed this. (2) BNIP3 knockdown alleviated LPS-induced injury and ferroptosis in H9c2 cells. (3) BNIP3 and BECN1 competed for BCL-2 binding, modulating ferroptosis-related signaling.
conclusionBCL-2 links the HIF1A/BNIP3 and BECN1/SLC7A11/GPX4 pathways, offering insights into septic myocardial injury mechanisms and potential therapeutic targets.
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