ArticleInternational journal of molecular medicine2018
Hypoxia induces endothelial‑mesenchymal transition in pulmonary vascular remodeling.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 98 citations in OpenAlex.
- A biphasic effect of alcohol on endothelial plasticity through regulation of endothelial-to-mesenchymal transition.American journal of physiology. Heart and circulatory physiology · 2026Article
- Imatinib Mesylate and Sirolimus Inhibit Vascular Fibroproliferative Remodeling in Pulmonary Vein Stenosis.Children (Basel, Switzerland) · 2026Article
- Absence of GDF15 Aggravates Pressure Overload-Induced Cardiac Remodelling in Mice Hallmarked by Perivascular Fibrosis and Signs of Endothelial-to-Mesenchymal Transition.International journal of molecular sciences · 2026Article
- Uterine Vulnerability to Environmental PMInternational journal of molecular sciences · 2026Article
- EndMT in vascular cognitive impairment and dementia: mechanisms, evidence gaps, and therapeutic opportunities.Molecular medicine (Cambridge, Mass.) · 2026Review
- COL3A1 promotes gastric cancer progression by activating PI3K/AKT signaling.Cancer gene therapy · 2026Article
- Understanding the Impact of Hypoxia on Pulmonary Artery Endothelial Cells in Chronic Thromboembolic Pulmonary Hypertension Patients.International journal of molecular sciences · 2026Article
- Roles of the Altitude-Adapted Immune Microenvironment in Pulmonary Vascular Remodeling in High-Altitude Pulmonary Hypertension: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2026Review
- Endothelial system dysregulation underlies keloid development and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- Curcumin Protected CoClFood science & nutrition · 2026Article
- Non-Coding RNAs in Obesity-Driven Vascular Dysfunction: Mechanisms, EndMT, and Translational Opportunities.Chonnam medical journal · 2026Review
- Endothelial-to-Mesenchymal Transition in Health and Disease: Molecular Insights and Therapeutic Implications.International journal of molecular sciences · 2025Review
- Iron enhances reactive oxygen species generation and initiates neutrophil extracellular traps formation on the endothelium to exacerbate stroke.Journal of cell communication and signaling · 2025Article
- The P4HA1/HIF1α feedback loop modulates endothelial dysfunction in pulmonary hypertension.Respiratory research · 2025Article
- Endothelial-to-mesenchymal transition in the central nervous system: A potential therapeutic target to combat age-related vascular fragility.The Journal of pharmacology and experimental therapeutics · 2025Review
- Derivation of Genetically Defined Murine Hepatoblastoma Cell Lines with Angiogenic Potential.Cancers · 2025Article
- Shifting Shapes: The Endothelial-to-Mesenchymal Transition as a Driver for Cancer Progression.International journal of molecular sciences · 2025Review
- Integrated Multi-Omics Analysis Reveals the Mechanisms of Intestinal Cell Injury Under Different Levels of Heat Stress.International journal of molecular sciences · 2025Article
- Role of MiR-542-3p/Integrin-Linked Kinase/Myocardin Signaling Axis in Hypoxic Pulmonary Hypertension.Pulmonary circulation · 2025Article
- Characterization of the Temporal Dynamics of the Endothelial-Mesenchymal-like Transition Induced by Soluble Factors from Dengue Virus Infection in Microvascular Endothelial Cells.International journal of molecular sciences · 2025Article
21 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well established that hypoxia induces epithelial‑mesenchymal transition in vitro and in vivo. However, the role of hypoxia in endothelial‑mesenchymal transition (EndMT), an important process in the pathogenesis of pulmonary hypertension, is not well‑characterized. The present study demonstrated a significant downregulation of the endothelial marker CD31 and its co‑localization with a mesenchymal marker, α‑smooth muscle actin (α‑SMA), in the intimal layer of small pulmonary arteries of rats exposed to chronic hypoxia. These results suggest a possible role of hypoxia in inducing EndMT in vivo. Consistent with these observations, pulmonary microvascular endothelial cells (PMVECs) cultured under hypoxic conditions exhibited a significant decrease in CD31 expression, alongside a marked increase in the expression of α‑SMA and two other mesenchymal markers, collagen (Col) 1A1 and Col3A1. In addition, hypoxia promoted the proliferation and migration of α‑SMA‑expressing mesenchymal‑like cells, but not of PMVECs. Of note, knockdown of hypoxia‑inducible factor 1α (HIF‑1α) effectively inhibited hypoxic induction of α‑SMA, Col1A1 and the transcription factor Twist1, while rescuing hypoxic suppression of CD31; these results suggest that HIF‑1α is essential for hypoxia‑induced EndMT and that it serves as an upstream regulator of Twist1. Mechanistically, HIF‑1α was identified to bind to the promoter of the Twist1 gene, thus activating Twist1 transcription and regulating EndMT. Collectively, the present results indicate that the HIF‑1α/Twist1 pathway has a critical role in mediating the effect of hypoxia‑induced EndMT in pulmonary arterial remodeling.
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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.