Evidence map›Paper›PMID 19210748›Full record

ReviewBritish journal of pharmacology2009

Role of nitrosative stress in the pathogenesis of diabetic vascular dysfunction.

Csaba Szabo

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 2 pooled it
12.2field-weighted citation impact, top 1% 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

75 citing papers in PubMed, 2 syntheses or guidelines pooled it, 161 citations in OpenAlex.

  1. Pooled it
  2. Growth factors for treating diabetic foot ulcers.The Cochrane database of systematic reviews · 2015
    Pooled it
  3. Article
  4. Review
  5. Review
  6. Multitargeted Effects ofInternational journal of molecular sciences · 2025
    Article
  7. Mechanistic underpinnings of AGEs-RAGE via DIAPH1 in ischemic, diabetic, and failing hearts.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Journal of diabetes research · 2023
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. The mitochondrial thioredoxin reductase system (TrxR2) in vascular endothelium controls peroxynitrite levels and tissue integrity.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  20. Endothelial dysfunction and body mass index: is there a role for plasma peroxynitrite?Beni-Suef University journal of basic and applied sciences · 2021
    Article

15 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Csaba SzaboDepartment of Anesthesiology, The University of Texas Medical Branch, Galveston, TX 77555-0833, USA. szabocsaba@aol.com
The University of Texas Medical Branch at Galveston · US

Funding

POLY (ADP RIBOSE) SYNTHETASE AND PEROXYNITRITE INDUCED CR01GM060915 · NIGMS · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SZABO, CSABA · 1999 to 2009
$1.9M
NIGMS NIH HHS R01 GM060915
6 · The paper itself

Abstract

Here we overview the role of reactive nitrogen species (nitrosative stress) and associated pathways in the pathogenesis of diabetic vascular complications. Increased extracellular glucose concentration, a principal feature of diabetes mellitus, induces a dysregulation of reactive oxygen and nitrogen generating pathways. These processes lead to a loss of the vascular endothelium to produce biologically active nitric oxide (NO), which impairs vascular relaxations. Mitochondria play a crucial role in this process: endothelial cells placed in increase extracellular glucose respond with a marked increase in mitochondrial superoxide formation. Superoxide, when combining with NO generated by the endothelial cells (produced by the endothelial isoform of NO synthase), leads to the formation of peroxynitrite, a cytotoxic oxidant. Reactive oxygen and nitrogen species trigger endothelial cell dysfunction through a multitude of mechanisms including substrate depletion and uncoupling of endothelial isoform of NO synthase. Another pathomechanism involves DNA strand breakage and activation of the nuclear enzyme poly(ADP-ribose) polymerase (PARP). PARP-mediated poly(ADP-ribosyl)ation and inhibition of glyceraldehyde-3-phosphate dehydrogenase importantly contributes to the development of diabetic vascular complications: it induces activation of multiple pathways of injury including activation of nuclear factor kappa B, activation of protein kinase C and generation of intracellular advanced glycation end products. Reactive species generation and PARP play key roles in the pathogenesis of 'glucose memory' and in the development of injury in endothelial cells exposed to alternating high/low glucose concentrations.

Indexed as

Aldehyde ReductaseAngiotensin IIAnimalsDiabetic AngiopathiesDrug Therapy, CombinationEndothelium, VascularEnzyme ActivationGlucoseGlycation End Products, AdvancedHumansOxidative StressPeroxynitrous AcidPoly Adenosine Diphosphate RiboseProtein Kinase CReactive Nitrogen SpeciesReactive Oxygen SpeciesAldehyde ReductaseAngiotensin IIGlucoseGlycation End Products, AdvancedPeroxynitrous AcidPoly Adenosine Diphosphate RiboseProtein Kinase CReactive Nitrogen SpeciesReactive Oxygen Species

Identifiers

PMID19210748
PMCPMC2697759
OpenAlexW1601356608

What OpenQuestion holds

Textmetadata
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.