Evidence map›Paper›PMID 28505880›Full record

ReviewRedox biology2017

Redox regulation of ischemic limb neovascularization - What we have learned from animal studies.

Reiko Matsui, Yosuke Watanabe, Colin E Murdoch

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Oxidative Stress Orchestrates MAPK and Nitric-Oxide Synthase Signal.International journal of molecular sciences · 2020
    Review
  6. Review
  7. Role of Glutaredoxin-1 and Glutathionylation in Cardiovascular Diseases.International journal of molecular sciences · 2020
    Review
  8. Redox RegulationAntioxidants & redox signaling · 2020
    Review
  9. Article
  10. Endothelial cell-specific redox gene modulation inhibits angiogenesis but promotes B16F0 tumor growth in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  11. Article
  12. Article
  13. Notch2 and Proteomic Signatures in Mouse Neointimal Lesion Formation.Arteriosclerosis, thrombosis, and vascular biology · 2018
    Article
  14. Article
  15. Article
  16. Article
  17. 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 3 institutions in 3 countries.

Reiko MatsuiVascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, USA. Electronic address: rmatsui@bu.edu.
Yosuke WatanabeDepartment of Internal Medicine II, University of Yamanashi, Faculty of Medicine, Japan.
Colin E MurdochAston Medical Research Institute, Aston Medical School, UK.
Aston University · GBBoston University · USUniversity of Yamanashi · JP

Funding

Project-005UL1TR001430 · NCATS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BAIR-MERRITT, MEGAN H, CENTER, DAVID M. · 2015 to 2024
$52.3M
Regulation of ischemic limb vascularization by glutaredoxin-1R01HL133013 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MATSUI, REIKO · 2016 to 2019
$1.6M
Regulation of ischemic vascularization by glutaredoxin-1 by agingR03AG051857 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MATSUI, REIKO · 2016 to 2017
$236k
Diabetes UK 16/0005453NCATS NIH HHS UL1 TR001430NHLBI NIH HHS R01 HL133013NIA NIH HHS R03 AG051857
6 · The paper itself

Abstract

Mouse hindlimb ischemia has been widely used as a model to study peripheral artery disease. Genetic modulation of the enzymatic source of oxidants or components of the antioxidant system reveal that physiological levels of oxidants are essential to promote the process of arteriogenesis and angiogenesis after femoral artery occlusion, although mice with diabetes or atherosclerosis may have higher deleterious levels of oxidants. Therefore, fine control of oxidants is required to stimulate vascularization in the limb muscle. Oxidants transduce cellular signaling through oxidative modifications of redox sensitive cysteine thiols. Of particular importance, the reversible modification with abundant glutathione, called S-glutathionylation (or GSH adducts), is relatively stable and alters protein function including signaling, transcription, and cytoskeletal arrangement. Glutaredoxin-1 (Glrx) is an enzyme which catalyzes reversal of GSH adducts, and does not scavenge oxidants itself. Glrx may control redox signaling under fluctuation of oxidants levels. In ischemic muscle increased GSH adducts through Glrx deletion improves in vivo limb revascularization, indicating endogenous Glrx has anti-angiogenic roles. In accordance, Glrx overexpression attenuates VEGF signaling in vitro and ischemic vascularization in vivo. There are several Glrx targets including HIF-1α which may contribute to inhibition of vascularization by reducing GSH adducts. These animal studies provide a caution that excess antioxidants may be counter-productive for treatment of ischemic limbs, and highlights Glrx as a potential therapeutic target to improve ischemic limb vascularization.

Indexed as

Disease Models, AnimalNeovascularization, PhysiologicAnimalsGlutaredoxinsGlutathioneHindlimbHumansHypoxia-Inducible Factor 1, alpha SubunitIschemiaMiceNeovascularization, PathologicOxidation-ReductionSignal TransductionVascular Endothelial Growth Factor AGlrx protein, mouseGlutaredoxinsGlutathioneHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseAngiogenesisGlutaredoxinGSH adductsIschemic limbOxidants

Identifiers

PMID28505880
PMCPMC5430575
OpenAlexW2611522974

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.