ArticleScientific reports2020
Mesenchymal-endothelial transition-derived cells as a potential new regulatory target for cardiac hypertrophy.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 44 citations in OpenAlex.
- Recovery From Heart Failure: Microvascular Mechanisms.Circulation · 2026Article
- Endothelial to mesenchymal transition in cardiovascular diseases: molecular insights and clinical perspectives.European heart journal · 2026Review
- Combined HIF-1α blockade and CHIR99021 treatment reverses pulmonary fibrosis via modulation endothelial-to-mesenchymal transition.iScience · 2025Article
- Transcription factor 4 maintains endothelial cell identity by inhibiting endothelial to mesenchymal transition.Nucleic acids research · 2025Article
- Hypertensive BPH/2J mice exhibit sex-specific heart failure progression and late-life microvascular rarefaction.American journal of physiology. Heart and circulatory physiology · 2025Article
- Endothelial Cpt1a Inhibits Neonatal Hyperoxia-Induced Pulmonary Vascular Remodeling by Repressing Endothelial-Mesenchymal Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Generation and characterisation of scalable and stable human pluripotent stem cell-derived microvascular-like endothelial cells for cardiac applications.Angiogenesis · 2024Article
- The role of autophagy in the progression of HIV infected cardiomyopathy.Frontiers in cell and developmental biology · 2024Review
- Myocardial Recovery versus Myocardial Regeneration: Mechanisms and Therapeutic Modulation.Methodist DeBakey cardiovascular journal · 2024Review
- Transflammation in tissue regeneration and response to injury: How cell-autonomous inflammatory signaling mediates cell plasticity.Advanced drug delivery reviews · 2023Review
- The Kaposi's sarcoma progenitor enigma: KSHV-induced MEndT-EndMT axis.Trends in molecular medicine · 2023Review
- Wnt4 is crucial for cardiac repair by regulating mesenchymal-endothelial transition via the phospho-JNK/JNK.Theranostics · 2022Article
- Oct4-dependent FoxC1 activation improves the survival and neovascularization of mesenchymal stem cells under myocardial ischemia.Stem cell research & therapy · 2021Article
- Sustained oxygenation accelerates diabetic wound healing by promoting epithelialization and angiogenesis and decreasing inflammation.Science advances · 2021Article
- Outside-in Signaling by Adventitial Fibroblasts.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Epithelial-to-Mesenchymal Transition in Fibrosis: Concepts and Targeting Strategies.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of Mesenchymal-endothelial transition (MEndoT) in cardiac hypertrophy is unclear. To determine the difference between MEndoT-derived and coronary endothelial cells is essential for understanding the revascularizing strategy in cardiac repair. Using lineage tracing we demonstrated that MEndoT-derived cells exhibit highly heterogeneous which were characterized with highly expression of endothelial markers such as vascular endothelial cadherin(VECAD) and occludin but low expression of Tek receptor tyrosine kinase(Tek), isolectin B4, endothelial nitric oxide synthase(eNOS), von Willebrand factor(vWF), and CD31 after cardiac hypertrophy. RNA-sequencing showed altered expression of fibroblast lineage commitment genes in fibroblasts undergoing MEndoT. Compared with fibroblasts, the expression of p53 and most endothelial lineage commitment genes were upregulated in MEndoT-derived cells; however, the further analysis indicated that MEndoT-derived cells may represent an endothelial-like cell sub-population. Loss and gain function study demonstrated that MEndoT-derived cells are substantial sources of neovascularization, which can be manipulated to attenuate cardiac hypertrophy and preserve cardiac function by improving the expression of endothelial markers in MEndoT-derived cells. Moreover, fibroblasts undergoing MEndoT showed significantly upregulated anti-hypertrophic factors and downregulated pro-hypertrophic factors. Therefore MEndoT-derived cells are an endothelial-like cell population that can be regulated to treat cardiac hypertrophy by improving neovascularization and altering the paracrine effect of fibroblasts.
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