Evidence map›Paper›PMID 19687749›Full record

ReviewJournal of cardiovascular pharmacology2009

S-Nitrosylation of cardiac ion channels.

Daniel R Gonzalez, Adriana Treuer, Qi-An Sun, Jonathan S Stamler, Joshua M Hare

Abstract readReview
In one paragraph

Review in Journal of cardiovascular pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

74 citing papers in PubMed, 137 citations in OpenAlex.

  1. Mechanotransduction-Driven Modulation ofInternational journal of molecular sciences · 2025
    Article
  2. Modulation of Redox-Sensitive Cardiac Ion Channels.Antioxidants (Basel, Switzerland) · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
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  12. Carbon monoxide activates large-conductance calcium-activated potassium channels of human cardiac fibroblasts through various mechanisms.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021
    Article
  13. Article
  14. Mechanisms underlying pathological CaPflugers Archiv : European journal of physiology · 2021
    Review
  15. Review
  16. Review
  17. Article
  18. Regulation of Ion Channel Function by Gas Molecules.Advances in experimental medicine and biology · 2021
    Review
  19. Review
  20. Review

14 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

5 authors at 3 institutions in 1 country.

Daniel R GonzalezInterdisciplinary Stem Cell Institute, Miller School of Medicine, University of Miami, Miami, FL 33101, USA.
Adriana Treuer
Qi-An Sun
Jonathan S Stamler
Joshua M Hare
University of Miami · USDuke University Hospital · USPulmonary Associates · US

Funding

Regulation of Beta-Adrenergic Receptor Signaling by S-NitrosylationP01HL075443 · NHLBI · DUKE UNIVERSITY · PI XIAO, KUNHONG · 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
OXIDATIVE STRESS IN HEART FAILURE: MECHANISMSR01HL065455 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARE, JOSHUA M · 2000 to 2008
$2.6M
Nitroso/redox balance in myocardial infarctionR01HL094849 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARE, JOSHUA M · 2009 to 2013
$2.2M
NHLBI NIH HHS P01 HL075443NHLBI NIH HHS P01-HL 75443NHLBI NIH HHS R01 HL059130NHLBI NIH HHS R01-HL059130NHLBI NIH HHS R01 HL065455NHLBI NIH HHS R01 HL094849NHLBI NIH HHS R01HL 65455NHLBI NIH HHS R01 HL94849
6 · The paper itself

Abstract

Nitric oxide (NO) exerts ubiquitous signaling via posttranslational modification of cysteine residues, a reaction termed S-nitrosylation. Important substrates of S-nitrosylation that influence cardiac function include receptors, enzymes, ion channels, transcription factors, and structural proteins. Cardiac ion channels subserving excitation-contraction coupling are potentially regulated by S-nitrosylation. Specificity is achieved in part by spatial colocalization of ion channels with nitric oxide synthases (NOSs), enzymatic sources of NO in biologic systems, and by coupling of NOS activity to localized calcium/second messenger concentrations. Ion channels regulate cardiac excitability and contractility in millisecond timescales, raising the possibility that NO-related species modulate heart function on a beat-to-beat basis. This review focuses on recent advances in understanding of NO regulation of the cardiac action potential and of the calcium release channel ryanodine receptor, which is crucial for the generation of force. S-Nitrosylation signaling is disrupted in pathological states in which the redox state of the cell is dysregulated, including ischemia, heart failure, and atrial fibrillation.

Indexed as

Protein Processing, Post-TranslationalAllosteric RegulationAnimalsAtrial FibrillationExcitation Contraction CouplingHeartHeart FailureHumansIon ChannelsLong QT SyndromeMyocardial ContractionMyocardiumNitric OxideNitrosationSignal TransductionIon ChannelsNitric Oxide

Identifiers

PMID19687749
PMCPMC3390783
OpenAlexW1963543097

What OpenQuestion holds

Textmetadata
LicenceTDM
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.