Evidence map›Paper›PMID 25399587›Full record

ReviewBiochemical Society transactions2014

Regulation of neovascularization by S-glutathionylation via the Wnt5a/sFlt-1 pathway.

Colin E Murdoch, Markus M Bachschmid, Reiko Matsui

Abstract readReview
In one paragraph

Review in Biochemical Society transactions, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Redox RegulationAntioxidants & redox signaling · 2020
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Expression of WNT5A in Idiopathic Pulmonary Fibrosis and Its Control by TGF-β and WNT7B in Human Lung Fibroblasts.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2016
    Article
  10. Article
  11. 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

3 authors at 2 institutions in 3 countries.

Colin E Murdoch*Vascular Medicine Section, Aston Medical School Aston University, Aston Triangle, Birmingham B47 ET, U.K.
Markus M Bachschmid†Vascular Biology Section, Boston University Medical School, Boston, MA 02118, U.S.A.
Reiko Matsui†Vascular Biology Section, Boston University Medical School, Boston, MA 02118, U.S.A.
Boston Medical Center · USAston University · GB

Funding

Redox Regulation of p21ras in AngiogenesisR37HL104017 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI COHEN, RICHARD A · 2010 to 2014
$2.2M
NHLBI NIH HHS HHSN268201000031CNHLBI NIH HHS R37 HL104017PHS HHS HHSN268201000031C
6 · The paper itself

Abstract

S-glutathionylation occurs when reactive oxygen or nitrogen species react with protein-cysteine thiols. Glutaredoxin-1 (Glrx) is a cytosolic enzyme which enzymatically catalyses the reduction in S-glutathionylation, conferring reversible signalling function to proteins with redox-sensitive thiols. Glrx can regulate vascular hypertrophy and inflammation by regulating the activity of nuclear factor κB (NF-κB) and actin polymerization. Vascular endothelial growth factor (VEGF)-induced endothelial cell (EC) migration is inhibited by Glrx overexpression. In mice overexpressing Glrx, blood flow recovery, exercise function and capillary density were significantly attenuated after hindlimb ischaemia (HLI). Wnt5a and soluble Fms-like tyrosine kinase-1 (sFlt-1) were enhanced in the ischaemic-limb muscle and plasma respectively from Glrx transgenic (TG) mice. A Wnt5a/sFlt-1 pathway had been described in myeloid cells controlling retinal blood vessel development. Interestingly, a Wnt5a/sFlt-1 pathway was found also to play a role in EC to inhibit network formation. S-glutathionylation of NF-κB components inhibits its activation. Up-regulated Glrx stimulated the Wnt5a/sFlt-1 pathway through enhancing NF-κB signalling. These studies show a novel role for Glrx in post-ischaemic neovascularization, which could define a potential target for therapy of impaired angiogenesis in pathological conditions including diabetes.

Indexed as

Neovascularization, PathologicAnimalsGlutaredoxinsGlutathioneHumansNF-kappa BProto-Oncogene ProteinsSignal TransductionUp-RegulationVascular Endothelial Growth Factor Receptor-1Wnt-5a ProteinWnt ProteinsFLT1 protein, humanGlutaredoxinsGlutathioneNF-kappa BProto-Oncogene ProteinsVascular Endothelial Growth Factor Receptor-1Wnt-5a ProteinWNT5A protein, humanWnt Proteins

Identifiers

PMID25399587
PMCPMC4934611
OpenAlexW1980967775

What OpenQuestion holds

Textmetadata
LicenceTDM
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.