ArticleJCI insight2017
Recapitulation of developmental mechanisms to revascularize the ischemic heart.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
46 citing papers in PubMed, 71 citations in OpenAlex.
- Article
- Necroptosis is a key contributor to impaired cardiac repair following myocardial infarction.Cell death & disease · 2026Article
- A miR-200b-Filamin A axis drives epicardial contribution to cardiogenesis.Scientific reports · 2026Article
- Review
- Linking Heat Stress to Impaired Cardiac Repair: The ER Stress-Angiogenesis Axis as a Critical Barrier.International journal of molecular sciences · 2026Review
- The RNA-binding protein SRSF3 controls epicardial formation by regulating splicing and proliferation.Development (Cambridge, England) · 2026Article
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- IDH2 lactylation promotes angiogenesis in murine diabetic myocardial infarction via blocking Cav1-eNOS interaction.Nature communications · 2025Article
- Cardiac mural cells are rate-limiting for coronary vascularization after heart injury.iScience · 2025Article
- Advances in Epicardial Biology: Insights from Development, Regeneration, and Human Cardiac Organoids.Journal of cardiovascular development and disease · 2025Review
- Transcription factor ETV1 promotes angiogenesis after myocardial infarction via activation of the VEGFA/VEGFR2/eNOS pathway.Frontiers in cardiovascular medicine · 2025Article
- flt1 inactivation promotes zebrafish cardiac regeneration by enhancing endothelial activity and limiting the fibrotic response.Development (Cambridge, England) · 2024Article
- Article
- Exploring the Function of Epicardial Cells Beyond the Surface.Circulation research · 2024Review
- Dynamic molecular signatures of acute myocardial infarction based on transcriptomics and metabolomics.Scientific reports · 2024Article
- Animal models to study cardiac regeneration.Nature reviews. Cardiology · 2024Review
- Identification and Validation of Diagnostic Model Based on Angiogenesis- and Epithelial Mesenchymal Transition-Related Genes in Myocardial Infarction.International journal of general medicine · 2024Article
- Clonal Expansion in Cardiovascular Pathology.JACC. Basic to translational science · 2024Review
- Loss of Histone Methyltransferase KMT2D Attenuates Angiogenesis in the Ischemic Heart by Inhibiting the Transcriptional Activation of VEGF-A.Journal of cardiovascular translational research · 2023Article
- Mechanisms regulating vascular and lymphatic regeneration in the heart after myocardial infarction.The Journal of pathology · 2023Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Restoring blood flow after myocardial infarction (MI) is essential for survival of existing and newly regenerated tissue. Endogenous vascular repair processes are deployed following injury but are poorly understood. We sought to determine whether developmental mechanisms of coronary vessel formation are intrinsically reactivated in the adult mouse after MI. Using pulse-chase genetic lineage tracing, we establish that de novo vessel formation constitutes a substantial component of the neovascular response, with apparent cellular contributions from the endocardium and coronary sinus. The adult heart reverts to its former hypertrabeculated state and repeats the process of compaction, which may facilitate endocardium-derived neovascularization. The capacity for angiogenic sprouting of the coronary sinus vein, the adult derivative of the sinus venosus, may also reflect its embryonic origin. The quiescent epicardium is reactivated and, while direct cellular contribution to new vessels is minimal, it supports the directional expansion of the neovessel network toward the infarcted myocardium. Thymosin β4, a peptide with roles in vascular development, was required for endocardial compaction, epicardial vessel expansion, and smooth muscle cell recruitment. Insight into pathways that regulate endogenous vascular repair, drawing on comparisons with development, may reveal novel targets for therapeutically enhancing neovascularization.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.