Evidence map›Paper›PMID 30120232›Full record

ArticleNature communications2018

SUMOylation of VEGFR2 regulates its intracellular trafficking and pathological angiogenesis.

Huanjiao Jenny Zhou, Zhe Xu, Zongren Wang, Haifeng Zhang, Zhen W Zhuang, Michael Simons, Wang Min

RetractedErratum issuedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

48 citing papers in PubMed, 88 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. SUMOylation is a Translatable Target in Hypoxic MNPs Regulating Retinal Vasculopathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Huanjiao Jenny ZhouInterdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, 10 Amistad St., New Haven, CT, 06520, USA. huanjiao.zhou@yale.edu.
Zhe XuInterdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, 10 Amistad St., New Haven, CT, 06520, USA.
Zongren WangInterdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, 10 Amistad St., New Haven, CT, 06520, USA.
Haifeng ZhangInterdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, 10 Amistad St., New Haven, CT, 06520, USA.
Zhen W ZhuangSection of Cardiology, Department of Internal Medicine, Yale University School of Medicine, 10 Amistad St., New Haven, CT, 06520, USA.
Michael SimonsSection of Cardiology, Department of Internal Medicine, Yale University School of Medicine, 10 Amistad St., New Haven, CT, 06520, USA.ORCID http://orcid.org/0000-0003-0348-7734
Wang MinInterdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, 10 Amistad St., New Haven, CT, 06520, USA. wang.min@yale.edu.ORCID http://orcid.org/0000-0002-2479-6096
Yale University · USSun Yat-sen University · CN

Funding

The role of signaling molecule AIP1 in pathological angiogenesisR01HL115148 · NHLBI · YALE UNIVERSITY · PI KYRIAKIDES, THEMIS R · 2013 to 2021
$3.6M
STRESS SIGNALING PATHWAYS LINKING ENDOTHELIAL INJURY TO GRAFT ARTERIOSCLEROSISR01HL109420 · NHLBI · YALE UNIVERSITY · PI POBER, JORDAN S · 2012 to 2020
$3.3M
CCM3-mediated exocytosis in pathogenesis of cerebral cavernous malformationR01HL136507 · NHLBI · YALE UNIVERSITY · PI STERN, DAVID F · 2017 to 2020
$1.9M
NHLBI NIH HHS R01 HL109420NHLBI NIH HHS R01 HL115148NHLBI NIH HHS R01 HL136507U.S. Department of Health & Human Services | NIH | Center for Scientific Review (CSR) HL109420U.S. Department of Health & Human Services | NIH | Center for Scientific Review (CSR) HL115148
6 · The paper itself

Abstract

Regulation of VEGFR2 represents an important mechanism for the control of angiogenesis. VEGFR2 activity can be regulated by post-translational modifications such as ubiquitination and acetylation. However, whether VEGFR2 can be regulated by SUMOylation has not been investigated. Here we show that endothelial-specific deletion of the SUMO endopeptidase SENP1 reduces pathological angiogenesis and tissue repair during hindlimb ischemia, and VEGF-induced angiogenesis in the cornea, retina, and ear. SENP1-deficient endothelial cells show increased SUMOylation of VEGFR2 and impaired VEGFR2 signalling. SUMOylation at lysine 1270 retains VEGFR2 in the Golgi and reduces its surface expression, attenuating VEGFR2-dependent signalling. Moreover, we find that SENP1 is downregulated and VEGFR2 hyper-SUMOylated in diabetic settings and that expression of a non-SUMOylated form of VEGFR2 rescues angiogenic defects in diabetic mice. These results show that VEGFR2 is regulated by deSUMOylation during pathological angiogenesis, and propose SENP1 as a potential therapeutic target for the treatment of diabetes-associated angiogenesis.

Indexed as

SumoylationAnimalsCorneaCysteine EndopeptidasesDiabetes MellitusEndopeptidasesGene DeletionGene Knock-In TechniquesGene SilencingGolgi ApparatusHumansHuman Umbilical Vein Endothelial CellsIntracellular SpaceMaleMice, Inbred C57BLMice, KnockoutCysteine EndopeptidasesEndopeptidasesSENP1 protein, humanSenp1 protein, mouseSUMO-1 ProteinVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID30120232
PMCPMC6098000
OpenAlexW2885978231

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.