ArticlePloS one2013
Contrasting roles of E2F2 and E2F3 in cardiac neovascularization.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Regulation of transglutaminase-2 and related miRNAs expression by calorie restriction in aorta of aging female mice.Molecular biology reports · 2025Article
- CCBE1 in Cardiac Development and Disease.Frontiers in genetics · 2022Review
- Critical functions of microRNA-30a-5p-E2F3 in cardiomyocyte apoptosis induced by hypoxia/reoxygenation.The Kaohsiung journal of medical sciences · 2021Article
- Spatiotemporal restriction of endothelial cell calcium signaling is required during leukocyte transmigration.The Journal of experimental medicine · 2021Article
- microRNA-377 Signaling Modulates Anticancer Drug-Induced Cardiotoxicity in Mice.Frontiers in cardiovascular medicine · 2021Article
- GRB10 and E2F3 as Diagnostic Markers of Osteoarthritis and Their Correlation with Immune Infiltration.Diagnostics (Basel, Switzerland) · 2020Article
- miR-378a-5p and miR-630 induce lens epithelial cell apoptosis in cataract via suppression of E2F3.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020Article
- Critical Roles of E2F3 in Growth and Musculo-skeletal Phenotype in Mice.International journal of medical sciences · 2019Article
- Glomerulocapillary miRNA response to HLA-class I antibody in vitro and in vivo.Scientific reports · 2017Article
- Crucial genes and pathways in chicken germ stem cell differentiation.The Journal of biological chemistry · 2015Article
- ERBB2 deficiency alters an E2F-1-dependent adaptive stress response and leads to cardiac dysfunction.Molecular and cellular biology · 2014Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Insufficient neovascularization, characterized by poor endothelial cell (EC) growth, contributes to the pathogenesis of ischemic heart disease and limits cardiac tissue preservation and regeneration. The E2F family of transcription factors are critical regulators of the genes responsible for cell-cycle progression and growth; however, the specific roles of individual E2Fs in ECs are not well understood. Here we investigated the roles of E2F2 and E2F3 in EC growth, angiogenesis, and their functional impact on myocardial infarction (MI). An endothelial-specific E2F3-deficient mouse strain VE-Cre; E2F3(fl/fl) was generated, and MI was surgically induced in VE-Cre; E2F3(fl/fl) and E2F2-null (E2F2 KO) mice and their wild-type (WT) littermates, VE-Cre; E2F3(+/+) and E2F2 WT, respectively. The cardiac function, infarct size, and vascular density were significantly better in E2F2 KO mice and significantly worse in VE-Cre; E2F3(fl/fl) mice than in their WT littermates. The loss of E2F2 expression was associated with an increase in the proliferation of ECs both in vivo and in vitro, while the loss of E2F3 expression led to declines in EC proliferation. Thus, E2F3 promotes while E2F2 suppresses ischemic cardiac repair through corresponding changes in EC proliferation; and differential targeting of specific E2F members may provide a novel strategy for therapeutic angiogenesis of ischemic heart disease.
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