Evidence map›Paper›PMID 27410748›Full record

ArticleBiophysical journal2016

Shear-Induced Nitric Oxide Production by Endothelial Cells.

Krishna Sriram, Justin G Laughlin, Padmini Rangamani, Daniel M Tartakovsky

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

69 citing papers in PubMed, 132 citations in OpenAlex.

  1. Trial
  2. Biophysics of lumen morphogenesis.Development (Cambridge, England) · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Vascular function in patients with advanced heart failure and continuous-flow or pulsatile ventricular assist devices.Clinical research in cardiology : official journal of the German Cardiac Society · 2025
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Fluid Shear Stress-Regulated Vascular Remodeling: Past, Present, and Future.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

9 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

4 authors at 1 institution in 1 country.

Krishna SriramDepartment of Mechanical and Aerospace Engineering, University of California-San Diego, La Jolla, California.
Justin G LaughlinDepartment of Mechanical and Aerospace Engineering, University of California-San Diego, La Jolla, California.
Padmini RangamaniDepartment of Mechanical and Aerospace Engineering, University of California-San Diego, La Jolla, California. Electronic address: padmini.rangamani@eng.ucsd.edu.
Daniel M TartakovskyDepartment of Mechanical and Aerospace Engineering, University of California-San Diego, La Jolla, California. Electronic address: dmt@ucsd.edu.
University of California, San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We present a biochemical model of the wall shear stress-induced activation of endothelial nitric oxide synthase (eNOS) in an endothelial cell. The model includes three key mechanotransducers: mechanosensing ion channels, integrins, and G protein-coupled receptors. The reaction cascade consists of two interconnected parts. The first is rapid activation of calcium, which results in formation of calcium-calmodulin complexes, followed by recruitment of eNOS from caveolae. The second is phosphorylation of eNOS by protein kinases PKC and AKT. The model also includes a negative feedback loop due to inhibition of calcium influx into the cell by cyclic guanosine monophosphate (cGMP). In this feedback, increased nitric oxide (NO) levels cause an increase in cGMP levels, so that cGMP inhibition of calcium influx can limit NO production. The model was used to predict the dynamics of NO production by an endothelial cell subjected to a step increase of wall shear stress from zero to a finite physiologically relevant value. Among several experimentally observed features, the model predicts a highly nonlinear, biphasic transient behavior of eNOS activation and NO production: a rapid initial activation due to the very rapid influx of calcium into the cytosol (occurring within 1-5 min) is followed by a sustained period of activation due to protein kinases.

Indexed as

Models, BiologicalShear StrengthBiomechanical PhenomenaCalciumCalmodulinEndothelial CellsEnzyme ActivationNitric OxideNitric Oxide Synthase Type IIICalciumCalmodulinNitric OxideNitric Oxide Synthase Type III

Identifiers

PMID27410748
PMCPMC4944664
OpenAlexW2346176709

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.