Evidence map›Paper›PMID 20203313›Full record

ReviewCirculation research2010

S-nitrosylation in cardiovascular signaling.

Brian Lima, Michael T Forrester, Douglas T Hess, Jonathan S Stamler

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03926741 (Methods to Identify and Treat Severe Asthma Patients Project 1), which is not on this map. Cited by 232 papers.

0numbers the graph read from it
0cells of the map it votes in
232citing papers in PubMed
27.9field-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.

NCT03926741 early_phase1completednot on this mapstarted 2019, after this paper: background citation

Methods to Identify and Treat Severe Asthma Patients Project 1: GSNOR Phenotyping and GSNO Challenge

TypeinterventionalSponsorJames ReynoldsRan2019 to 2024Enrolled48ConditionsAsthmaArmsGSNO Challenge
3 · Its place in the literature

Who cites it

232 citing papers in PubMed, 490 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Dysregulated ProteinCirculation research · 2025
    Article
  6. Soluble guanylyl cyclase, the NO receptor, drives vasorelaxation via endothelial S-nitrosation.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Article
  8. The Ever-Expanding Influence of the Endothelial Nitric Oxide Synthase.Basic & clinical pharmacology & toxicology · 2025
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Brian LimaDepartment of Surgery, Duke University Medical Center, Durham, NC, USA.
Michael T Forrester
Douglas T Hess
Jonathan S Stamler
Duke University · US

Funding

Regulation of Beta-Adrenergic Receptor Signaling by S-NitrosylationP01HL075443 · NHLBI · DUKE UNIVERSITY · PI STAMLER, JONATHAN S. · 2004 to 2019
$26.1M
Redox Signalling by Nitric Oxide in Skeletal MuscleR01HL059130 · NHLBI · DUKE UNIVERSITY · PI STAMLER, JONATHAN S. · 1997 to 2011
$3.1M
Red Blood Cell S-nitrosothiols and OxygenationR01HL091876 · NHLBI · DUKE UNIVERSITY · PI STAMLER, JONATHAN S. · 2009 to 2012
$1.6M
Restoration and Function of S-nitrosothiol in Stored BloodR01HL095463 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI STAMLER, JONATHAN S. · 2009 to 2012
$1.5M
Regulation of Cardiac Adrenergic Function by S-nitrosylationR01HL096673 · NHLBI · DUKE UNIVERSITY · PI STAMLER, JONATHAN S. · 2009 to 2009
$10k
NHLBI NIH HHS P01 HL075443NHLBI NIH HHS P01-HL075443NHLBI NIH HHS R01 HL059130NHLBI NIH HHS R01-HL059130NHLBI NIH HHS R01 HL091876NHLBI NIH HHS R01-HL091876NHLBI NIH HHS R01 HL095463NHLBI NIH HHS R01 HL096673NHLBI NIH HHS R01-HL096673
6 · The paper itself

Abstract

Well over 2 decades have passed since the endothelium-derived relaxation factor was reported to be the gaseous molecule nitric oxide (NO). Although soluble guanylyl cyclase (which generates cyclic guanosine monophosphate, cGMP) was the first identified receptor for NO, it has become increasingly clear that NO exerts a ubiquitous influence in a cGMP-independent manner. In particular, many, if not most, effects of NO are mediated by S-nitrosylation, the covalent modification of a protein cysteine thiol by an NO group to generate an S-nitrosothiol (SNO). Moreover, within the current framework of NO biology, endothelium-derived relaxation factor activity (ie, G protein-coupled receptor-mediated, or shear-induced endothelium-derived NO bioactivity) is understood to involve a central role for SNOs, acting both as second messengers and signal effectors. Furthermore, essential roles for S-nitrosylation have been implicated in virtually all major functions of NO in the cardiovascular system. Here, we review the basic biochemistry of S-nitrosylation (and denitrosylation), discuss the role of S-nitrosylation in the vascular and cardiac functions of NO, and identify current and potential clinical applications.

Indexed as

Protein Processing, Post-TranslationalSignal TransductionAnimalsApoptosisCardiovascular DiseasesCardiovascular SystemCyclic GMPEndothelium-Dependent Relaxing FactorsEndothelium, VascularHumansInflammationMyocardiumNeovascularization, PhysiologicNitric OxideS-NitrosothiolsVascular ResistanceCyclic GMPEndothelium-Dependent Relaxing FactorsNitric OxideS-Nitrosothiols

Identifiers

PMID20203313
PMCPMC2891248
OpenAlexW2143004446

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.