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Here, we demonstrate that after myocardial infarction, adult Bmi1<jats:sup>+<\/jats:sup>(B lymphoma Mo-MLV insertion region 1 homolog [PCGF4]) cardiac cells are a key progenitor-like population in cardiac neovascularization during ventricular remodeling.<\/jats:p><\/jats:sec><jats:sec><jats:title>Approach and Results\u2014<\/jats:title><jats:p>These cells, which have a strong in vivo differentiation bias, are a mixture of endothelial- and mesenchymal-related cells with in vitro spontaneous endothelial cell differentiation capacity. Genetic lineage tracing analysis showed that heart-resident Bmi1<jats:sup>+<\/jats:sup>progenitor cells proliferate after acute myocardial infarction and differentiate to generate de novo cardiac vasculature. In a mouse model of induced myocardial infarction, genetic ablation of these cells substantially deteriorated both heart angiogenesis and the ejection fraction, resulting in an ischemic-dilated cardiac phenotype.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions\u2014<\/jats:title><jats:p>These findings imply that endothelial-related Bmi1<jats:sup>+<\/jats:sup>progenitor cells are necessary for injury-induced neovascularization in adult mouse heart and highlight these cells as a suitable therapeutic target for preventing dysfunctional left ventricular remodeling after injury.<\/jats:p><\/jats:sec>","DOI":"10.1161\/atvbaha.118.310778","type":"journal-article","created":{"date-parts":[[2018,6,21]],"date-time":"2018-06-21T09:00:57Z","timestamp":1529571657000},"page":"2160-2173","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":17,"title":["Bmi1-Progenitor Cell Ablation Impairs the Angiogenic Response to Myocardial 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