ArticleThe American journal of pathology2019
Endothelial Hypoxia-Inducible Factor-1α Is Required for Vascular Repair and Resolution of Inflammatory Lung Injury through Forkhead Box Protein M1.
Article in The American journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 60 citations in OpenAlex.
- Posttranslational modifications in regulating Notch signaling pathway and tumor angiogenesis: from molecular mechanisms to therapeutic applications.Journal of molecular cell biology · 2026Review
- Hypoxia inducible factors regulate pneumovirus replication by enhancing innate immune sensing.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Cardiac fibroblast Foxm1 deficiency prevents pressure overload-induced cardiac remodeling via the Usp10/MKK6-p38γ MAPK axis.Cell death and differentiation · 2026Review
- Mechanisms Underlying Altitude-Induced and Group 3 Pulmonary Hypertension.International journal of molecular sciences · 2026Review
- The Unexpected Protective Role of Thrombosis in Lung Injury via Endothelial Alox15.Circulation research · 2026Article
- Comparison of pharmacovigilance and mechanism analysis of the vascular toxicity caused by platin-based chemotherapy: integration of FAERS analysis, network pharmacology, and endothelial validation.Therapeutic advances in drug safety · 2026Article
- HIF-1α: a bridge connecting sepsis and acute respiratory distress syndrome.European journal of medical research · 2025Review
- Review
- AREGMolecular medicine (Cambridge, Mass.) · 2025Article
- Control of inflammatory lung injury and repair by metabolic signaling in endothelial cells.Current opinion in hematology · 2025Review
- Advances in acute respiratory distress syndrome: focusing on heterogeneity, pathophysiology, and therapeutic strategies.Signal transduction and targeted therapy · 2025Review
- Macrophage A2aR Alleviates LPS-Induced Vascular Endothelial Injury and Inflammation via Inhibiting M1 Polarisation and Oxidative Stress.Journal of cellular and molecular medicine · 2025Article
- Mechanisms and therapeutic prospects of hypoxia-inducible factor 1-alpha in acute kidney injury: a systematic review.Frontiers in cell and developmental biology · 2025Review
- Unraveling the deadly dance: endothelial cells and neutrophils in sepsis-induced acute lung injury/acute respiratory distress syndrome.Frontiers in cell and developmental biology · 2025Review
- Neutrophils Extracellular Traps Impair Lung Endothelial Proliferation in Sepsis via PLK1 Inhibition and Cell Cycle Arrest.Journal of inflammation research · 2025Article
- Expression and Regulation of Hypoxia-Inducible Factor Signalling in Acute Lung Inflammation.Cells · 2024Review
- Review
- Therapeutic targeting of hypoxia inducible factor in acute respiratory distress syndrome.The Journal of physiology · 2024Review
- Review
- Mechanisms of pulmonary endothelial barrier dysfunction in acute lung injury and acute respiratory distress syndrome.Chinese medical journal pulmonary and critical care medicine · 2024Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
Endothelial barrier dysfunction is a central factor in the pathogenesis of persistent lung inflammation and protein-rich edema formation, the hallmarks of acute respiratory distress syndrome. However, little is known about the molecular mechanisms that are responsible for vascular repair and resolution of inflammatory injury after sepsis challenge. Herein, we show that hypoxia-inducible factor-1α (HIF-1α), expressed in endothelial cells (ECs), is the critical transcriptional factor mediating vascular repair and resolution of inflammatory lung injury. After sepsis challenge, HIF-1α but not HIF-2α expression was rapidly induced in lung vascular ECs, and mice with EC-restricted disruption of Hif1α (Hif1a
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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.