Evidence map›Paper›PMID 23708369›Full record

ArticleBiophysical journal2013

In silico modeling of shear-stress-induced nitric oxide production in endothelial cells through systems biology.

Andrew Koo, David Nordsletten, Renato Umeton, Beracah Yankama, Shiva Ayyadurai, Guillermo García-Cardeña, C Forbes Dewey

Open access · hybridAbstract read
In one paragraph

Article in Biophysical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 3 pooled it
–field-weighted citation impact, top 95% 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

27 citing papers in PubMed, 3 syntheses or guidelines pooled it, 1 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Omics of endothelial cell dysfunction in sepsis.Vascular biology (Bristol, England) · 2022
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. The profiles of soluble adhesion molecules in the "great obstetrical syndromes"The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2019
    Article
  18. Review
  19. Article
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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

7 authors at 3 institutions in 2 countries.

Andrew KooDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
David Nordsletten
Renato Umeton
Beracah Yankama
Shiva Ayyadurai
Guillermo García-Cardeña
C Forbes Dewey
Massachusetts Institute of Technology · USBrigham and Women's Hospital · USKing's College London · GB

Funding

The Role of Glycocalyx in MechanotransductionR01HL090856 · NHLBI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI DEWEY, C FORBES · 2009 to 2010
$934k
NHLBI NIH HHS R01 HL090856NHLBI NIH HHS R01HL090856
6 · The paper itself

Abstract

Nitric oxide (NO) produced by vascular endothelial cells is a potent vasodilator and an antiinflammatory mediator. Regulating production of endothelial-derived NO is a complex undertaking, involving multiple signaling and genetic pathways that are activated by diverse humoral and biomechanical stimuli. To gain a thorough understanding of the rich diversity of responses observed experimentally, it is necessary to account for an ensemble of these pathways acting simultaneously. In this article, we have assembled four quantitative molecular pathways previously proposed for shear-stress-induced NO production. In these pathways, endothelial NO synthase is activated 1), via calcium release, 2), via phosphorylation reactions, and 3), via enhanced protein expression. To these activation pathways, we have added a fourth, a pathway describing actual NO production from endothelial NO synthase and its various protein partners. These pathways were combined and simulated using CytoSolve, a computational environment for combining independent pathway calculations. The integrated model is able to describe the experimentally observed change in NO production with time after the application of fluid shear stress. This model can also be used to predict the specific effects on the system after interventional pharmacological or genetic changes. Importantly, this model reflects the up-to-date understanding of the NO system, providing a platform upon which information can be aggregated in an additive way.

Indexed as

Models, BiologicalStress, PhysiologicalSystems BiologyAnimalsCalciumEndothelial CellsEndothelium, VascularHumansNitric OxideNitric Oxide Synthase Type IIIPhosphorylationShear StrengthSignal TransductionCalciumNitric OxideNitric Oxide Synthase Type III

Identifiers

PMID23708369
PMCPMC3660651
OpenAlexW1568209455

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.