Evidence map›Paper›PMID 21536106›Full record

ReviewBiochimica et biophysica acta2012

Regulation of cardiovascular cellular processes by S-nitrosylation.

Ivonne Hernandez Schulman, Joshua M Hare

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 53 citations in OpenAlex.

  1. Trial
  2. Review
  3. 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
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Can Serum Nitrosoproteome Predict Longevity of Aged Women?International journal of molecular sciences · 2020
    Article
  10. Article
  11. Article
  12. Rethinking Endothelial Dysfunction as a Crucial Target in Fighting Heart Failure.Mayo Clinic proceedings. Innovations, quality & outcomes · 2019
    Review
  13. Article
  14. Article
  15. ROS signaling and redox biology in endothelial cells.Cellular and molecular life sciences : CMLS · 2015
    Review
  16. Article
  17. Article
  18. Article
  19. Cardiac stem cells: biology and clinical applications.Antioxidants & redox signaling · 2014
    Review
  20. 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.

Ivonne Hernandez SchulmanInterdisciplinary Stem Cell Institute, University of Miami Miller School of Medicine, Miami, FL, USA.
Joshua M Hare
University of Miami · US

Funding

Mesenchymal Stem Cell CardiomyoplastyU54HL081028 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI MARBAN, EDUARDO · 2005 to 2009
$12.1M
Cardioprotective Effect of Growth Hormone Releasing HormoneR01HL107110 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARE, JOSHUA M · 2011 to 2020
$5.9M
Cellular Cardiomyoplasty for Chronic Heart FailureR01HL084275 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARE, JOSHUA M · 2007 to 2016
$3.8M
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
Autologous Adult Myocardial Cardioblasts to Treat Ischemic Heart FailureP20HL101443 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARE, JOSHUA M · 2010 to 2011
$1.5M
NHLBI NIH HHS P20 HL101443NHLBI NIH HHS R01 HL065455NHLBI NIH HHS R01 HL084275NHLBI NIH HHS R01 HL094849NHLBI NIH HHS R01 HL107110NHLBI NIH HHS R01 HL65455NHLBI NIH HHS U54 HL081028
6 · The paper itself

Abstract

backgroundNitric oxide (NO), a highly versatile signaling molecule, exerts a broad range of regulatory influences in the cardiovascular system that extends from vasodilation to myocardial contractility, angiogenesis, inflammation, and energy metabolism. Considerable attention has been paid to deciphering the mechanisms for such diversity in signaling. S-nitrosylation of cysteine thiols is a major signaling pathway through which NO exerts its actions. An emerging concept of NO pathophysiology is that the interplay between NO and reactive oxygen species (ROS), the nitroso/redox balance, is an important regulator of cardiovascular homeostasis. SCOPE OF REVIEW: ROS react with NO, limit its bioavailability, and compete with NO for binding to the same thiol in effector molecules. The interplay between NO and ROS appears to be tightly regulated and spatially confined based on the co-localization of specific NO synthase (NOS) isoforms and oxidative enzymes in unique subcellular compartments. NOS isoforms are also in close contact with denitrosylases, leading to crucial regulation of S-nitrosylation. MAJOR

conclusionsNitroso/redox balance is an emerging regulatory pathway for multiple cells and tissues, including the cardiovascular system. Studies using relevant knockout models, isoform specific NOS inhibitors, and both in vitro and in vivo methods have provided novel insights into NO- and ROS-based signaling interactions responsible for numerous cardiovascular disorders. GENERAL SIGNIFICANCE: An integrated view of the role of nitroso/redox balance in cardiovascular pathophysiology has significant therapeutic implications. This is highlighted by human studies where pharmacologic manipulation of oxidative and nitrosative pathways exerted salutary effects in patients with advanced heart failure. This article is part of a Special Issue entitled Regulation of Cellular Processes by S-nitrosylation.

Indexed as

AnimalsCalciumCardiovascular DiseasesCardiovascular SystemCell Physiological PhenomenaCysteineHeart FailureHumansMyocardiumNitric OxideNitric Oxide SynthaseNitrosationOxidation-ReductionOxidative StressReactive Oxygen SpeciesSignal TransductionCalciumCysteineNitric OxideNitric Oxide SynthaseReactive Oxygen Species

Identifiers

PMID21536106
PMCPMC5509026
OpenAlexW2012124023

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.