ArticleApoptosis : an international journal on programmed cell death2025
Endothelial HMGB1-AIM2 axis worsens myocardial ischemia-reperfusion injury by regulating endothelial pyroptosis.
Article in Apoptosis : an international journal on programmed cell death, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The trial behind it
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Who cites it
9 citing papers in PubMed.
- Silencing of HAVCR2 Attenuates Skeletal Muscle Ischemia-Reperfusion Injury by Inhibiting Oxidative Stress.Biochemical genetics · 2026Article
- Inflammaging and cytokine-driven cardiovascular senescence in age-related myocardial infarction: mechanisms, biomarkers, and precision immunotherapy strategies.Biogerontology · 2026Review
- Sevoflurane Alleviates Myocardial Ischemia-Reperfusion Injury via the HMGB1/ACSL4 Pathway to Suppress Ferroptosis.Journal of biochemical and molecular toxicology · 2026Article
- The role of HMGB1 in vascular endothelial cells.Apoptosis : an international journal on programmed cell death · 2026Review
- Potential Relationship Between Ferroptosis and Pyroptosis in Myocardial Ischemia/Reperfusion Injury: Molecular Mechanisms and Therapeutic Targets.Reviews in cardiovascular medicine · 2026Review
- Programmed Cell Death of Endothelial Cells in Ischemic Heart Disease: Mechanism and Potential Cell and Gene Therapeutic Prospects.Bioengineering (Basel, Switzerland) · 2026Review
- Damage-Associated Molecular Patterns in Perioperative Anesthesia Care: A Clinical Perspective.Anesthesia research · 2026Article
- Involvement of the pyroptosis-HMGB1 axis in systemic diseases.Frontiers in cell and developmental biology · 2026Review
- The immune-cardiovascular metabolic circuitry in myocardial ischemia-reperfusion injury: from metabolic signal release to spatiotemporal reprogramming.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
This study investigates mechanisms related to endothelial cells in myocardial ischaemia-reperfusion (I/R) injury, focusing on the role of high-mobility group box 1 (HMGB1) protein in these cells. Using a murine model, we observed elevated levels of HMGB1 in both the heart and circulation following I/R, with a portion originating from cardiac vascular endothelial cells and cardiomyocytes. Endothelial cell-specific HMGB1 knockout preserved cardiac function after I/R by reducing infarct size, mitigating myocardial damage, maintaining endothelial cell barrier function, and attenuating inflammatory and oxidative stress responses. Single-cell analysis revealed that HMGB1 endothelial knockout altered cardiac cell composition by decreasing the proportion of endothelial cells with high fatty acid-binding protein 4 expression. Mechanistically, HMGB1 endothelial knockout significantly inhibited the expression of absent in melanoma 2 (AIM2)-associated inflammasome- and pyroptosis-related proteins after I/R, whereas AIM2 overexpression exacerbated myocardial injury, inflammation, and the expression of pyroptosis-related proteins. Our findings demonstrate that the endothelial HMGB1-AIM2 axis worsens I/R injury by regulating endothelial cell pyroptosis, suggesting a novel pathway involved in microcirculatory dysfunction during myocardial I/R injury.
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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.