ArticleJournal of molecular and cellular cardiology2011
The role of E2F-1 and downstream target genes in mediating ischemia/reperfusion injury in vivo.
Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 25 citations in OpenAlex.
- Exercise volume modulates cardiac protection in a type 2 diabetic rat model: differential effects of high- and low-volume moderate-intensity endurance exercise training on diabetic cardiomyopathy.Cardiovascular diabetology. Endocrinology reports · 2026Article
- The E2F family: a ray of dawn in cardiomyopathy.Molecular and cellular biochemistry · 2025Review
- Interdependent Nuclear Co-Trafficking of ASPP1 and p53 Aggravates Cardiac Ischemia/Reperfusion Injury.Circulation research · 2023Article
- Loss of Rbl2 (Retinoblastoma-Like 2) Exacerbates Myocardial Ischemia/Reperfusion Injury.Journal of the American Heart Association · 2022Article
- Inhibition of DYRK1a Enhances Cardiomyocyte Cycling After Myocardial Infarction.Circulation research · 2022Article
- Differential gene responses 3 days following infarction in the fetal and adolescent sheep heart.Physiological genomics · 2020Article
- Cell Cycle Proteins as Key Regulators of Postmitotic Cell Death.The Yale journal of biology and medicine · 2019Review
- E2f1 deletion attenuates infarct-induced ventricular remodeling without affecting O-GlcNAcylation.Basic research in cardiology · 2019Article
- FoxO transcription factors in cancer metabolism.Seminars in cancer biology · 2018Review
- E2F1 Suppresses Oxidative Metabolism and Endothelial Differentiation of Bone Marrow Progenitor Cells.Circulation research · 2018Article
- Wnt11 regulates cardiac chamber development and disease during perinatal maturation.JCI insight · 2017Article
- Posttranscriptional regulation of FOXO expression: microRNAs and beyond.British journal of pharmacology · 2017Review
- Cardiac-specific ablation of the E3 ubiquitin ligase Mdm2 leads to oxidative stress, broad mitochondrial deficiency and early death.PloS one · 2017Article
- The Long Noncoding RNA Landscape of the Ischemic Human Left Ventricle.Circulation. Cardiovascular genetics · 2017Article
- Signaling Pathways in Cardiac Myocyte Apoptosis.BioMed research international · 2016Review
- Article
- Redox regulation of FoxO transcription factors.Redox biology · 2015Review
- E2F1-dependent miR-421 regulates mitochondrial fragmentation and myocardial infarction by targeting Pink1.Nature communications · 2015Article
- E2F1-regulated miR-30b suppresses Cyclophilin D and protects heart from ischemia/reperfusion injury and necrotic cell death.Cell death and differentiation · 2015Article
- E2F1 suppresses cardiac neovascularization by down-regulating VEGF and PlGF expression.Cardiovascular research · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
E2Fs are a family of transcription factors that regulate proliferation, differentiation and apoptosis in many cell types. E2F-1 is the prototypical E2F and the family member that has most often been implicated in also mediating apoptosis. To better understand the role of E2F-1 in mediating cardiomyocyte injury we initially analyzed E2F family member expression after ischemia/reperfusion (I/R) in vivo or simulated ischemia in vitro. I/R injury in vivo caused a 3.4-fold increase specifically in E2F-1 protein levels. Expression of other E2F family members did not change. To establish the role of E2F-1 in I/R we examined the response of germline deleted E2F-1 mice to I/R injury. Infarct size as a percentage of the area at risk was decreased 39.8% in E2F-1(-/-) mice compared to E2F-1(+/+) controls. Interestingly, expression of classic, E2F-1 apoptotic target genes was not altered in E2F-1 null cardiomyocytes after I/R. However, upregulation of the primary member of the Forkhead family of transcription factors, FoxO-1a, was attenuated. Consistent, with a role for FoxO-1a as an important target of E2F-1 in I/R, a number of proapoptotic FoxO-1a target genes were also altered. These results suggest that E2F-1 and FoxO-1a belong to a complex transcriptional network that may modulate myocardial cell death during I/R injury.
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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.