Evidence map›Paper›PMID 25341896›Full record

ArticleCardiovascular research2014

E2F1 suppresses cardiac neovascularization by down-regulating VEGF and PlGF expression.

Min Wu, Junlan Zhou, Min Cheng, Chan Boriboun, Dauren Biyashev, Hong Wang, Alexander Mackie, Tina Thorne, Jonathan Chou, Yiping Wu and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.7field-weighted citation impact, top 27% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  4. Observational
  5. The E2F family: a ray of dawn in cardiomyopathy.Molecular and cellular biochemistry · 2025
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  6. Oxidative medicine and cellular longevity · 2025
    Article
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  11. Exosomes Derived from E2F1International journal of nanomedicine · 2023
    Article
  12. Review
  13. Ablation of lncRNATheranostics · 2021
    Article
  14. The Role of the VEGF Family in Coronary Heart Disease.Frontiers in cardiovascular medicine · 2021
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

21 authors at 10 institutions in 2 countries.

Min WuDepartment of Plastic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China Department of Medicine-Cardiology, Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, 303 E Chicago Ave., Tarry 14-721, Chicago, IL 60611, USA.
Junlan ZhouDepartment of Medicine-Cardiology, Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, 303 E Chicago Ave., Tarry 14-721, Chicago, IL 60611, USA.
Min ChengDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Chan BoribounDepartment of Medicine-Cardiology, Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, 303 E Chicago Ave., Tarry 14-721, Chicago, IL 60611, USA.
Dauren BiyashevDepartment of Medicine-Cardiology, Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, 303 E Chicago Ave., Tarry 14-721, Chicago, IL 60611, USA.
Hong WangDepartment of Medicine-Cardiology, Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, 303 E Chicago Ave., Tarry 14-721, Chicago, IL 60611, USA.
Alexander MackieDepartment of Medicine-Cardiology, Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, 303 E Chicago Ave., Tarry 14-721, Chicago, IL 60611, USA.
Tina ThorneDepartment of Medicine-Cardiology, Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, 303 E Chicago Ave., Tarry 14-721, Chicago, IL 60611, USA.
Jonathan ChouDepartment of Medicine-Cardiology, Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, 303 E Chicago Ave., Tarry 14-721, Chicago, IL 60611, USA.
Yiping WuDepartment of Plastic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Zhishui ChenOrgan Transplantation Institute, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Qinghua LiuInstitute for Medical Biology and Hubei Provincial Key Laboratory for Protection and Application of Special Plants in Wuling Area of China, College of Life Sciences, South-Central University for Nationalities, Wuhan, Hubei, China.
Hongbin YanCardiology Department, Cardiovascular Institute and Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Ya YangDepartment of Echocardiography, Beijing Anzhen Hospital, Capital Medical University and Beijing Institute of Heart, Lung and Blood Vessel Disease, Beijing, China.
Chunfa JieDepartment of Surgery, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Yao-Liang TangDepartment of Medicine, Vascular Biology Center, Medical College of Georgia/Georgia Regents University, Augusta, GA, USA.
Ting C ZhaoDepartment of Surgery, Roger Williams Medical Center, Boston University Medical School, Boston University, Providence, RI, USA.
Robert N TaylorDepartment of Obstetrics and Gynecology, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA.
Raj KishoreCenter for Translational Medicine, Temple University School of Medicine, Philadelphia, PA, USA.
Douglas W LosordoDepartment of Medicine-Cardiology, Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, 303 E Chicago Ave., Tarry 14-721, Chicago, IL 60611, USA.
Gangjian QinDepartment of Medicine-Cardiology, Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, 303 E Chicago Ave., Tarry 14-721, Chicago, IL 60611, USA g-qin@northwestern.edu.
Northwestern University · USHuazhong University of Science and Technology · CNAugusta University · USCapital Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNRoger Williams Medical Center · USSouth Central University for Nationalities · CNTemple University · USTongji Hospital · CNWake Forest University · US

Funding

CXCR4 and ckit signaling in BM progenitor cell recruitment in the ischemic heartR01HL113541 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI QIN, GANGJIAN · 2012 to 2015
$1.5M
E2F1 in Cardiac NeovascularizationR01HL093439 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI QIN, GANGJIAN · 2010 to 2013
$1.5M
NHLBI NIH HHS HL093439NHLBI NIH HHS HL113541NHLBI NIH HHS R01 HL093439NHLBI NIH HHS R01 HL113541
6 · The paper itself

Abstract

aimsThe E2F transcription factors are best characterized for their roles in cell-cycle regulation, cell growth, and cell death. Here we investigated the potential role of E2F1 in cardiac neovascularization. METHODS AND

resultsWe induced myocardial infarction (MI) by ligating the left anterior descending artery in wild-type (WT) and E2F1(-/-) mice. E2F1(-/-) mice demonstrated a significantly better cardiac function and smaller infarct sizes than WT mice. At infarct border zone, capillary density and endothelial cell (EC) proliferation were greater, apoptotic ECs were fewer, levels of VEGF and placental growth factor (PlGF) were higher, and p53 level was lower in E2F1(-/-) than in WT mice. Blockade of VEGF receptor 2 (VEGFR2) signalling with the selective inhibitor SU5416 or with the VEGFR2-blocking antibody DC101 abolished the differences between E2F1(-/-) mice and WT mice in cardiac function, infarct size, capillary density, EC proliferation, and EC apoptosis. In vitro, hypoxia-induced VEGF and PlGF up-regulation was significantly greater in E2F1(-/-) than in WT cardiac fibroblasts, and E2F1 overexpression suppressed PlGF up-regulation in both WT and p53(-/-) cells; however, VEGF up-regulation was suppressed only in WT cells. E2F1 interacted with and stabilized p53 under hypoxic conditions, and both E2F1 : p53 binding and the E2F1-induced suppression of VEGF promoter activity were absent in cells that expressed an N-terminally truncated E2F1 mutant.

conclusionE2F1 limits cardiac neovascularization and functional recovery after MI by suppressing VEGF and PlGF up-regulation through p53-dependent and -independent mechanisms, respectively.

Indexed as

Neovascularization, PhysiologicAnimalsCells, CulturedCoronary VesselsE2F1 Transcription FactorFibroblastsGene Expression RegulationHeartHypoxiaMaleMice, KnockoutMyocardial InfarctionMyocardiumPlacenta Growth FactorPregnancy ProteinsProteasome Endopeptidase ComplexE2f1 protein, mouseE2F1 Transcription FactorKdr protein, mousePgf protein, mousePlacenta Growth FactorPregnancy ProteinsProteasome Endopeptidase ComplexTumor Suppressor Protein p53Vascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseVascular Endothelial Growth Factor Receptor-2E2F1Heartp53PlGFVEGF

Identifiers

PMID25341896
PMCPMC4296109
OpenAlexW2110450264

What OpenQuestion holds

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Registered trials

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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.