ArticleNature2014
Mesenchymal-endothelial transition contributes to cardiac neovascularization.
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Article in Nature, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 234 papers, 1 of them a synthesis that pooled it.
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234citing papers in PubMed, 1 pooled it
18.9field-weighted citation impact, top 1% of its field
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Who cites it
234 citing papers in PubMed, 1 synthesis or guideline pooled it, 360 citations in OpenAlex.
- Rational transplant timing and dose of mesenchymal stromal cells in patients with acute myocardial infarction: a meta-analysis of randomized controlled trials.Stem cell research & therapy · 2017Pooled it
- A regenerative fibroblast competence field supports multiple cell fates in adult skin regeneration.bioRxiv : the preprint server for biology · 2026Article
- Decoding fibroblast activation: Transcriptional networks in hepatic stellate cells and across fibrotic organs (Review).International journal of molecular medicine · 2026Review
- Cardiac fibroblast deletion of PTBP1 modulates the profibrotic response by alternative splicing.Nature communications · 2026Article
- Recovery From Heart Failure: Microvascular Mechanisms.Circulation · 2026Article
- TAK1 drives inflammatory fibroblast acquisition and shapes myocardial infarction responses in male mice.Nature communications · 2026Article
- An Inhibitory Aptamer Against PDGF-C Overcomes Anti-VEGF Refractoriness and Reduces Choroidal Neovascularization and Fibrosis.Investigative ophthalmology & visual science · 2026Article
- Single-cell lineage tracing identifies hemogenic endothelial cells in the adult mouse bone marrow.eLife · 2026Article
- Endothelial to mesenchymal transition in cardiovascular diseases: molecular insights and clinical perspectives.European heart journal · 2026Review
- Targeting Cardiac Fibroblast Plasticity for Antifibrotic and Regenerative Therapy in Heart Failure.Cells · 2026Review
- Combined HIF-1α blockade and CHIR99021 treatment reverses pulmonary fibrosis via modulation endothelial-to-mesenchymal transition.iScience · 2025Article
- IGF1-mediated mesenchymal-endothelial transition as a potential regulatory target in calcific aortic valve disease.BMC medicine · 2025Article
- Endothelial cell in tumor angiogenesis: Origins, mechanisms, and therapeutic implication.Genes & diseases · 2025Review
- Transcription factor 4 maintains endothelial cell identity by inhibiting endothelial to mesenchymal transition.Nucleic acids research · 2025Article
- Single-cell lineage tracing identifies hemogenic endothelial cells in the adult mouse bone marrow.bioRxiv : the preprint server for biology · 2025Article
- The role of cellular senescence in cardiovascular disease.Cell death discovery · 2025Review
- Article
- Single-Short Partial Reprogramming of the Endothelial Cells Decreases Blood Pressure via Attenuation of EndMT in Hypertensive Mice.Circulation research · 2025Article
- Pyruvate kinase splice variants in fibroblasts influence cardiac remodeling after myocardial infarction in male mice.Journal of molecular and cellular cardiology · 2025Article
- Current perspectives on regenerative potential of mesenchymal stem cells in alleviating cardiac injuries: Molecular pathways and therapeutic enhancement.World journal of stem cells · 2025Review
174 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Eric UbilDepartment of Cell Biology &Physiology, School of Medicine, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
Jinzhu Duan1] Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [2] Cardiovascular Research Laboratory, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [3] Eli and Edythe Broad Institute of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, California 90095, USA [4] Department of Molecular, Cell and Developmental Biology, College of Letters and Sciences, University of California, Los Angeles, California 90095, USA [5] Jonsson Comprehensive Cancer Center, University of California, Los Angeles, California 90095, USA [6] Molecular Biology Institute, University of California, Los Angeles, California 90095, USA.
Indulekha C L Pillai1] Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [2] Cardiovascular Research Laboratory, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [3] Eli and Edythe Broad Institute of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, California 90095, USA [4] Department of Molecular, Cell and Developmental Biology, College of Letters and Sciences, University of California, Los Angeles, California 90095, USA [5] Jonsson Comprehensive Cancer Center, University of California, Los Angeles, California 90095, USA [6] Molecular Biology Institute, University of California, Los Angeles, California 90095, USA.
Manuel Rosa-Garrido1] Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [2] Cardiovascular Research Laboratory, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [3] Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [4] Department of Physiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA.
Yong WuDivision of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA.
Francesca BargiacchiDepartment of Pharmacology, School of Medicine, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
Yan Lu1] Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [2] Cardiovascular Research Laboratory, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [3] Eli and Edythe Broad Institute of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, California 90095, USA [4] Department of Molecular, Cell and Developmental Biology, College of Letters and Sciences, University of California, Los Angeles, California 90095, USA [5] Jonsson Comprehensive Cancer Center, University of California, Los Angeles, California 90095, USA [6] Molecular Biology Institute, University of California, Los Angeles, California 90095, USA.
Seta Stanbouly1] Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [2] Cardiovascular Research Laboratory, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [3] Eli and Edythe Broad Institute of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, California 90095, USA [4] Department of Molecular, Cell and Developmental Biology, College of Letters and Sciences, University of California, Los Angeles, California 90095, USA [5] Jonsson Comprehensive Cancer Center, University of California, Los Angeles, California 90095, USA [6] Molecular Biology Institute, University of California, Los Angeles, California 90095, USA.
Jie Huang1] Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [2] Cardiovascular Research Laboratory, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [3] Eli and Edythe Broad Institute of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, California 90095, USA [4] Department of Molecular, Cell and Developmental Biology, College of Letters and Sciences, University of California, Los Angeles, California 90095, USA [5] Jonsson Comprehensive Cancer Center, University of California, Los Angeles, California 90095, USA [6] Molecular Biology Institute, University of California, Los Angeles, California 90095, USA.
Mauricio RojasDepartment of Medicine, McAllister Heart Institute, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
Thomas M Vondriska1] Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [2] Cardiovascular Research Laboratory, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [3] Molecular Biology Institute, University of California, Los Angeles, California 90095, USA [4] Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [5] Department of Physiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA.
Enrico Stefani1] Cardiovascular Research Laboratory, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [2] Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [3] Department of Physiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA.
Arjun Deb1] Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [2] Cardiovascular Research Laboratory, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA [3] Eli and Edythe Broad Institute of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, California 90095, USA [4] Department of Molecular, Cell and Developmental Biology, College of Letters and Sciences, University of California, Los Angeles, California 90095, USA [5] Jonsson Comprehensive Cancer Center, University of California, Los Angeles, California 90095, USA [6] Molecular Biology Institute, University of California, Los Angeles, California 90095, USA.
University of California, Los Angeles · USUniversity of North Carolina at Chapel Hill · US
Funding
PREDOCTORAL TRAINING IN PHARMACOLOGICAL SCIST32GM007040 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI NICHOLAS, ROBERT A · 1985 to 2019
$6.0MRevealing Cardiovascular Stress Regulation beyond the Diffraction LimitR01HL088640 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI STEFANI, ENRICO · 2007 to 2011
$5.3MDynamics of Cardiac Nuclei in Heart DiseaseR01HL105699 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI VONDRISKA, THOMAS M. · 2011 to 2025
$5.0MRole of Wnts in Cardiac RepairR01HL102190 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DEB, ARJUN · 2010 to 2014
$1.8MNHLBI NIH HHS HL088640NHLBI NIH HHS HL105699NHLBI NIH HHS R01 HL088640NHLBI NIH HHS R01 HL102190NHLBI NIH HHS R01HL102190NHLBI NIH HHS R01 HL105699NIGMS NIH HHS T32 GM007040
Abstract
Endothelial cells contribute to a subset of cardiac fibroblasts by undergoing endothelial-to-mesenchymal transition, but whether cardiac fibroblasts can adopt an endothelial cell fate and directly contribute to neovascularization after cardiac injury is not known. Here, using genetic fate map techniques, we demonstrate that cardiac fibroblasts rapidly adopt an endothelial-cell-like phenotype after acute ischaemic cardiac injury. Fibroblast-derived endothelial cells exhibit anatomical and functional characteristics of native endothelial cells. We show that the transcription factor p53 regulates such a switch in cardiac fibroblast fate. Loss of p53 in cardiac fibroblasts severely decreases the formation of fibroblast-derived endothelial cells, reduces post-infarct vascular density and worsens cardiac function. Conversely, stimulation of the p53 pathway in cardiac fibroblasts augments mesenchymal-to-endothelial transition, enhances vascularity and improves cardiac function. These observations demonstrate that mesenchymal-to-endothelial transition contributes to neovascularization of the injured heart and represents a potential therapeutic target for enhancing cardiac repair.
Indexed as
Cell TransdifferentiationNeovascularization, PhysiologicAnimalsCoronary VesselsEndothelial CellsFemaleFibroblastsIn Vitro TechniquesMaleMesodermMiceMyocardial IschemiaTumor Suppressor Protein p53Tumor Suppressor Protein p53
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