ArticleInternational journal of molecular sciences2017
Endothelial Mesenchymal Transition in Hypoxic Microvascular Endothelial Cells and Paracrine Induction of Cardiomyocyte Apoptosis Are Mediated via TGFβ₁/SMAD Signaling.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
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- PKM2-Driven Lactate Overproduction Triggers Endothelial-To-Mesenchymal Transition in Ischemic Flap via Mediating TWIST1 Lactylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Cell-cell interactions in the heart: advanced cardiac models and omics technologies.Stem cell research & therapy · 2024Review
- Experimental Models to Study Endothelial to Mesenchymal Transition in Myocardial Fibrosis and Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Epigallocatechin-3-Gallate Attenuates Myocardial Dysfunction via Inhibition of Endothelial-to-Mesenchymal Transition.Antioxidants (Basel, Switzerland) · 2023Article
- Tissue Reactions and Mechanism in Cardiovascular Diseases Induced by Radiation.International journal of molecular sciences · 2022Review
- Yes-associated protein promotes endothelial-to-mesenchymal transition of endothelial cells in choroidal neovascularization fibrosis.International journal of ophthalmology · 2022Article
- The Roles of Cardiac Fibroblasts and Endothelial Cells in Myocarditis.Frontiers in cardiovascular medicine · 2022Review
- Article
- Endothelial-Mesenchymal Transition or Functional Tissue Regeneration - Two Outcomes of Heart Remodeling.Physiological research · 2021Review
- A promising field: regulating imbalance of EndMT in cardiovascular diseases.Cell cycle (Georgetown, Tex.) · 2021Review
- Autocrine Signaling in Cardiac Remodeling: A Rich Source of Therapeutic Targets.Journal of the American Heart Association · 2021Review
- Communication Between Cardiomyocytes and Fibroblasts During Cardiac Ischemia/Reperfusion and Remodeling: Roles of TGF-β, CTGF, the Renin Angiotensin Axis, and Non-coding RNA Molecules.Frontiers in physiology · 2021Review
- The Impact of Inflammatory Immune Reactions of the Vascular Niche on Organ Fibrosis.Frontiers in pharmacology · 2021Review
- Forensic interrogation of diabetic endothelitis in cardiovascular diseases and clinical translation in heart failure.World journal of cardiology · 2020Review
- Increased miR-7641 Levels in Peritoneal Hyalinizing Vasculopathy in Long-Term Peritoneal Dialysis Patients.International journal of molecular sciences · 2020Article
- Endothelial cell-cardiomyocyte crosstalk in heart development and disease.The Journal of physiology · 2020Review
- A Signaling Crosstalk between BMP9 and HGF/c-Met Regulates Mouse Adult Liver Progenitor Cell Survival.Cells · 2020Article
- Long Noncoding RNA SOX2-OT Exacerbates Hypoxia-Induced Cardiomyocytes Injury by Regulating miR-27a-3p/TGFCardiovascular therapeutics · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac remodeling plays a crucial role in the development of heart failure after mycocardial infarction. Besides cardiomyocytes, endothelial cells are recognized to contribute to cardiac remodeling. We now investigated processes of endothelial mesenchymal transition (EndoMT) in microvascular endothelial cells of rat (MVEC) under hypoxia and paracrine effects on ventricular cardiomyocytes of adult rat. Exposure of MVECs to hypoxia/reoxygenation enhanced TGFβ/SMAD signaling, since phosphorylation, and thus activation, of SMAD1/5 and SMAD2 increased. This increase was blocked by inhibitors of TGFβ receptor types ALK1 or ALK5. Exposure of ventricular cardiomyocytes to conditioned medium from hypoxic/reoxygenated MVECs enhanced SMAD2 phosphorylation and provoked apoptosis in cardiomyoyctes. Both were blocked by ALK5 inhibition. To analyze autocrine effects of hypoxic TGFβ signaling we investigated EndoMT in MVECs. After 3 days of hypoxia the mesenchymal marker protein α-smooth muscle actin (α-SMA), and the number of α-SMA- and fibroblast specific protein 1 (FSP1)-positive cells increased in MVECs cultures. This was blocked by ALK5 inhibition. Similarly, TGFβ₁ provoked enhanced expression of α-SMA and FSP1 in MVECs. In conclusion, hypoxia provokes EndoMT in MVECs via TGFβ₁/SMAD2 signaling. Furthermore, release of TGFβ₁ from MVECs acts in a paracrine loop on cardiomyocytes and provokes apoptotic death. Thus, in myocardial infarction hypoxic endothelial cells may contribute to cardiac remodeling and heart failure progression by promotion of cardiac fibrosis and cardiomyocytes death.
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Registered trials
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