Evidence map›Paper›PMID 24440455›Full record

ReviewJournal of molecular and cellular cardiology2014

Signaling by S-nitrosylation in the heart.

Elizabeth Murphy, Mark Kohr, Sara Menazza, Tiffany Nguyen, Alicia Evangelista, Junhui Sun, Charles Steenbergen

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. [Exogenous nitric oxide suppresses KSheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2026
    Article
  4. Article
  5. Dysregulated ProteinCirculation research · 2025
    Article
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  8. Torpid 13-lined ground squirrel liver mitochondria resist anoxia-reoxygenation despite high levels of protein damage.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2023
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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 2 institutions in 1 country.

Elizabeth MurphyCardiac Physiology Laboratory, Systems Biology Center, NHLBI, NIH, USA. Electronic address: murphy1@mail.nih.gov.
Mark KohrCardiac Physiology Laboratory, Systems Biology Center, NHLBI, NIH, USA; Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD, USA.
Sara MenazzaCardiac Physiology Laboratory, Systems Biology Center, NHLBI, NIH, USA.
Tiffany NguyenCardiac Physiology Laboratory, Systems Biology Center, NHLBI, NIH, USA.
Alicia EvangelistaCardiac Physiology Laboratory, Systems Biology Center, NHLBI, NIH, USA.
Junhui SunCardiac Physiology Laboratory, Systems Biology Center, NHLBI, NIH, USA.
Charles SteenbergenDepartment of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD, USA.
Center for Systems Biology · USJohns Hopkins University · US

Funding

Mechanisms of cardiac ischemia-reperfusion injury and cardioprotectionZIAHL002066 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI MURPHY, ELIZABETH · 2009 to 2025
$20.4M
Role of S-nitrosylation in regulating cardiac function and diseaseZIAHL006059 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI MURPHY, ELIZABETH · 2010 to 2025
$7.2M
ELEVATED CALCIUM AND MYOCARDIAL ISCHEMIC INJURYR01HL039752 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI STEENBERGEN, CHARLES · 1993 to 2019
$6.6M
S-Nitrosylation and CardioprotectionR00HL114721 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI KOHR, MARK JEFFREY · 2015 to 2017
$729k
S-Nitrosylation and CardioprotectionK99HL114721 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI KOHR, MARK JEFFREY · 2013 to 2014
$215k
Intramural NIH HHS ZIA HL002066Intramural NIH HHS ZIA HL006059NHLBI NIH HHS K99 HL114721NHLBI NIH HHS R00 HL114721NHLBI NIH HHS R01 HL039752
6 · The paper itself

Abstract

Nitric oxide is a gaseous signaling molecule that is well-known for the Nobel prize-winning research that defined nitric oxide as a physiological regulator of blood pressure in the cardiovascular system. Nitric oxide can signal via the classical pathway involving activation of guanylyl cyclase or by a post-translational modification, referred to as S-nitrosylation (SNO) that can occur on cysteine residues of proteins. As proteins with cysteine residues are common, this allows for amplification of the nitric oxide signaling. This review will focus on the possible mechanisms through which SNO can alter protein function in cardiac cells, and the role of SNO occupancy in these mechanisms. The specific mechanisms that regulate protein SNO, including redox-dependent processes, will also be discussed. This article is part of a Special Issue entitled "Redox Signalling in the Cardiovascular System".

Indexed as

HeartAnimalsHumansNitric OxideOxidation-ReductionProtein Processing, Post-TranslationalSignal TransductionS-NitrosothiolsNitric OxideS-NitrosothiolsCardioportectionNitric oxideOxidation

Identifiers

PMID24440455
PMCPMC4214076
OpenAlexW2091174988

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.