ArticleNature communications2021
Cardiomyocytes stimulate angiogenesis after ischemic injury in a ZEB2-dependent manner.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 113 citations in OpenAlex.
- Role of ZEB1 in angiogenesis and therapeutic potential (Review).International journal of molecular medicine · 2026Review
- The Zinc-Senescence Axis in Skin Aging and Wound Healing: A Narrative Review.International journal of molecular sciences · 2026Review
- ZEB2 SUMOylation in Cardiac Fibroblast Drives Post-Infarction Cardiac Remodeling through CtBP1-Associated repression of Nr4a1.iScience · 2026Article
- Integrated Bioinformatics and Experimental Validation of Post-Translational Modification-Related Biomarkers in Myocardial Ischemia-Reperfusion Injury.Journal of cardiovascular translational research · 2026Article
- Advances in Living Myocardial Slice Technology for Heart Failure Research.Current heart failure reports · 2026Review
- Review
- Proteomic landscape analysis of undifferentiated pleomorphic sarcoma.Genome medicine · 2026Article
- YBX1 promotes angiogenesis after myocardial infarction by stabilizing HIF1α mRNA via miScience · 2026Article
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- Role of Macrophage-Related Genes GAS7 and ZEB2 in Acute Myocardial Infarction Pathogenesis.Human mutation · 2026Article
- Integrated multi-omics profiling of the early post-infarct heart reveals a hub gene network associated with myeloid-driven inflammation.Frontiers in cardiovascular medicine · 2026Article
- Mesenchymal stem cell-derived exosomes in myocardial infarction repair: therapeutic potential and scaffold-based delivery strategies.Frontiers in pharmacology · 2026Review
- AAV6-based ZEB2 delivery promotes cardiomyocyte dedifferentiation in adult human myocardium.Cardiovascular research · 2025Article
- Heterogeneity and characteristic changes in cardiomyocytes and non‑cardiomyocytes following myocardial infarction: Insights from single‑cell sequencing analysis (Review).Molecular medicine reports · 2025Review
- An infusible decellularized extracellular matrix material binds to vasculature in infarcted myocardium and induces pro-reparative gene expression following acute myocardial infarction through inherent avidity and bioactive signaling.bioRxiv : the preprint server for biology · 2025Article
- Circular RNA Cdr1as Modulates Macrophage-Mediated Cardiac Reparative Function.Circulation research · 2025Article
- Cardiac Development, Cellular Composition and Function: From Regulatory Mechanisms to Applications.Cells · 2025Review
- A robust method for assessing mitochondrial function in healthy and diseased frozen cardiac tissue.Communications biology · 2025Article
- Endothelial PRMT7 prevents dysfunction, promotes revascularization and enhances cardiac recovery post-myocardial infarction.Experimental & molecular medicine · 2025Article
- Zebrafish Models of Induced Lymphangiogenesis: Current Advancements and Therapeutic Discovery.Pharmaceuticals (Basel, Switzerland) · 2025Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The disruption in blood supply due to myocardial infarction is a critical determinant for infarct size and subsequent deterioration in function. The identification of factors that enhance cardiac repair by the restoration of the vascular network is, therefore, of great significance. Here, we show that the transcription factor Zinc finger E-box-binding homeobox 2 (ZEB2) is increased in stressed cardiomyocytes and induces a cardioprotective cross-talk between cardiomyocytes and endothelial cells to enhance angiogenesis after ischemia. Single-cell sequencing indicates ZEB2 to be enriched in injured cardiomyocytes. Cardiomyocyte-specific deletion of ZEB2 results in impaired cardiac contractility and infarct healing post-myocardial infarction (post-MI), while cardiomyocyte-specific ZEB2 overexpression improves cardiomyocyte survival and cardiac function. We identified Thymosin β4 (TMSB4) and Prothymosin α (PTMA) as main paracrine factors released from cardiomyocytes to stimulate angiogenesis by enhancing endothelial cell migration, and whose regulation is validated in our in vivo models. Therapeutic delivery of ZEB2 to cardiomyocytes in the infarcted heart induces the expression of TMSB4 and PTMA, which enhances angiogenesis and prevents cardiac dysfunction. These findings reveal ZEB2 as a beneficial factor during ischemic injury, which may hold promise for the identification of new therapies.
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