Herrero, DiegoCañon, SusanaPelacho, BeatrizSalvador-Bernaldez, MariaAguilar, SusanaPogontke, CristinaCarmona, Rosa MariaSalvador, Jesus MariaPerez-Pomares, Jose MariaKlein, Ophir DavidProsper, FelipeJimenez-Borreguero, Luis JesusBernad, Antonio2023-01-252023-01-252018-09Herrero D, Cañón S, Pelacho B, Salvador-Bernáldez M, Aguilar S, Pogontke C, et al. Bmi1-Progenitor Cell Ablation Impairs the Angiogenic Response to Myocardial Infarction. Arterioscler Thromb Vasc Biol. 2018 Sep;38(9):2160-2173.http://hdl.handle.net/10668/12630Cardiac progenitor cells reside in the heart in adulthood, although their physiological relevance remains unknown. Here, we demonstrate that after myocardial infarction, adult Bmi1+ (B lymphoma Mo-MLV insertion region 1 homolog [PCGF4]) cardiac cells are a key progenitor-like population in cardiac neovascularization during ventricular remodeling. Approach and Results- 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+ 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. Conclusions- These findings imply that endothelial-related Bmi1+ 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.encell differentiationlymphomamyocardial infarctionphenotypeventricular remodelingCentro Andaluz de Nanomedicina y Biotecnología (BIONAND)AnimalsCells, CulturedDisease Models, AnimalFemaleHumansMaleMiceMice, TransgenicMyocardial InfarctionMyocytes, CardiacNeovascularization, PathologicPolycomb Repressive Complex 1Proto-Oncogene Proteins c-kitStem CellsTranscription FactorsVentricular Remodelingresearch article29930004Restricted AccessInfarto de miocardioCélulas progenitorasNeovascularización fisiológicaRemodelación ventricularCélulas endotelialesCélulas madre mesenquimatosas10.1161/ATVBAHA.118.3107781524-4636PMC6202133https://www.ahajournals.org/doi/pdf/10.1161/ATVBAHA.118.310778https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6202133/pdf