Evidence map›Paper›PMID 21742028›Full record

ArticleFree radical biology & medicine2011

Modeling of biopterin-dependent pathways of eNOS for nitric oxide and superoxide production.

Saptarshi Kar, Mahendra Kavdia

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.9field-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

16 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Review
  3. The role and mechanisms of microvascular damage in the ischemic myocardium.Cellular and molecular life sciences : CMLS · 2023
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Aerobic Exercises Induce Antioxidant Pathways Activation in Rats.International journal of preventive medicine · 2020
    Article
  9. Article
  10. Review
  11. New horizons in pulmonary arterial hypertension therapies.European respiratory review : an official journal of the European Respiratory Society · 2013
    Review
  12. Article
  13. Article
  14. Nitric oxide synthases in heart failure.Antioxidants & redox signaling · 2013
    Review
  15. Article
  16. 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

2 authors at 1 institution in 1 country.

Saptarshi KarDepartment of Biomedical Engineering, Wayne State University, Detroit, MI 48202, USA. s.kar@wayne.edu
Mahendra Kavdia
Wayne State University · US

Funding

Nitric Oxide-Superoxide Interactions in Endothelial Cell DysfunctionR01HL084337 · NHLBI · WAYNE STATE UNIVERSITY · PI KAVDIA, MAHENDRA · 2008 to 2012
$1.3M
NHLBI NIH HHS R01 HL084337
6 · The paper itself

Abstract

Endothelial dysfunction is associated with increase in oxidative stress and low NO bioavailability. The endothelial NO synthase (eNOS) uncoupling is considered an important factor in endothelial cell oxidative stress. Under increased oxidative stress, the eNOS cofactor tetrahydrobiopterin (BH(4)) is oxidized to dihydrobiopterin, which competes with BH(4) for binding to eNOS, resulting in eNOS uncoupling and reduction in NO production. The importance of the ratio of BH(4) to oxidized biopterins versus absolute levels of total biopterin in determining the extent of eNOS uncoupling remains to be determined. We have developed a computational model to simulate the kinetics of the biochemical pathways of eNOS for both NO and O(2)(•-) production to understand the roles of BH(4) availability and total biopterin (TBP) concentration in eNOS uncoupling. The downstream reactions of NO, O(2)(•-), ONOO(-), O(2), CO(2), and BH(4) were also modeled. The model predicted that a lower [BH(4)]/[TBP] ratio decreased NO production but increased O(2)(•-) production from eNOS. The NO and O(2)(•-) production rates were independent above 1.5μM [TBP]. The results indicate that eNOS uncoupling is a result of a decrease in [BH(4)]/[TBP] ratio, and a supplementation of BH(4) might be effective only when the [BH(4)]/[TBP] ratio increases. The results from this study will help us understand the mechanism of endothelial dysfunction.

Indexed as

BiocatalysisBiopterinsCarbon DioxideEndothelial CellsEnzyme ActivationKineticsModels, ChemicalNitric OxideNitric Oxide Synthase Type IIIOxidation-ReductionOxidative StressOxygenPeroxynitrous AcidProtein BindingSuperoxides7,8-dihydrobiopterinBiopterinsCarbon DioxideNitric OxideNitric Oxide Synthase Type IIIOxygenPeroxynitrous AcidsapropterinSuperoxides

Identifiers

PMID21742028
PMCPMC3184605
OpenAlexW2073963062

What OpenQuestion holds

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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.