ArticleThe Journal of clinical investigation2017
Preexisting endothelial cells mediate cardiac neovascularization after injury.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers.
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Who cites it
129 citing papers in PubMed.
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- From cell atlases to mechanisms: bridging scRNA-seq discovery with in vivo genetics.The EMBO journal · 2026Article
- Hypoxia differentially affects coronary vessel formation during heart development.Cardiovascular research · 2026Article
- Cardiac-targeted delivery of miRNA via antioxidant nanozymes ameliorates cardiac dysfunction and fibrosis after myocardial infarction.Journal of nanobiotechnology · 2026Article
- Recovery From Heart Failure: Microvascular Mechanisms.Circulation · 2026Article
- Endothelial soluble APP/APLP2 promote heart repair through KIT-mediated angiogenesis.Science advances · 2026Article
- Local gene editing of fibroblasts in tumors reveals a new cancer-associated fibroblast state.The Journal of experimental medicine · 2026Article
- Review
- Temporal inhibition of ADAM17 in fibroblasts reduces stiffness and promotes vascularization following myocardial infarction.Cardiovascular research · 2026Article
- Efficient in vivo targeting of the myocardial scar using Moloney murine leukaemia virus complexed with nanoparticles.The Journal of physiology · 2026Article
- Tenascin CNature communications · 2026Article
- Endothelial cell in tumor angiogenesis: Origins, mechanisms, and therapeutic implication.Genes & diseases · 2025Review
- CCL28 contributes to angiogenesis and cardiac repair through CCR10Nature communications · 2025Article
- The role of cellular senescence in cardiovascular disease.Cell death discovery · 2025Review
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- Resolving fibrosis by stimulating HSC-dependent extracellular matrix degradation.Science translational medicine · 2025Article
- Discovery of a Linked Constellation of Gene Expression Revealed by Local Editing of Fibroblasts in Tumors.bioRxiv : the preprint server for biology · 2025Article
- Zebrafish Models of Induced Lymphangiogenesis: Current Advancements and Therapeutic Discovery.Pharmaceuticals (Basel, Switzerland) · 2025Review
69 more citing papers are in PubMed but not listed here.
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Authors and funding
23 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms that promote the generation of new coronary vasculature during cardiac homeostasis and after injury remain a fundamental and clinically important area of study in the cardiovascular field. Recently, it was reported that mesenchymal-to-endothelial transition (MEndoT) contributes to substantial numbers of coronary endothelial cells after myocardial infarction. Therefore, the MEndoT has been proposed as a paradigm mediating neovascularization and is considered a promising therapeutic target in cardiac regeneration. Here, we show that preexisting endothelial cells mainly beget new coronary vessels in the adult mouse heart, with essentially no contribution from other cell sources through cell-lineage transdifferentiation. Genetic-lineage tracing revealed that cardiac fibroblasts expand substantially after injury, but do not contribute to the formation of new coronary blood vessels, indicating no contribution of MEndoT to neovascularization. Moreover, genetic-lineage tracing with a pulse-chase labeling strategy also showed that essentially all new coronary vessels in the injured heart are derived from preexisting endothelial cells, but not from other cell lineages. These data indicate that therapeutic strategies for inducing neovascularization should not be based on targeting presumptive lineage transdifferentiation such as MEndoT. Instead, preexisting endothelial cells appear more likely to be the therapeutic target for promoting neovascularization and driving heart regeneration after injury.
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