Evidence map›Paper›PMID 28493997›Full record

ArticlePloS one2017

Adenosine A1 receptor activation increases myocardial protein S-nitrosothiols and elicits protection from ischemia-reperfusion injury in male and female hearts.

Qin Shao, Kevin M Casin, Nathan Mackowski, Elizabeth Murphy, Charles Steenbergen, Mark J Kohr

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. GSNOR deletion differentially alters age-related cardiac function in a sex-dependent manner.American journal of physiology. Heart and circulatory physiology · 2026
    Article
  3. Article
  4. Dysregulated ProteinCirculation research · 2025
    Article
  5. Review
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  9. Article
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  11. Review
  12. Article
  13. Review
  14. Postconditioning with Nitrates Protects Against Myocardial Reperfusion Injury: A New Use for an Old Pharmacological Agent.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Mechanisms involved in adenosine pharmacological preconditioning-induced cardioprotection.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018
    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

6 authors at 2 institutions in 2 countries.

Qin ShaoDepartment of Cardiology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Kevin M CasinDepartment of Environmental Health and Engineering, Bloomberg School of Public Health, Whiting School of Engineering, Johns Hopkins University, Baltimore, Maryland, United States of America.
Nathan MackowskiDepartment of Environmental Health and Engineering, Bloomberg School of Public Health, Whiting School of Engineering, Johns Hopkins University, Baltimore, Maryland, United States of America.
Elizabeth MurphySystems Biology Center, National Heart, Lung and Blood Institute, Bethesda, Maryland, United States of America.
Charles SteenbergenDepartment of Pathology, School of Medicine, Johns Hopkins University, Baltimore, Maryland, United States of America.
Mark J KohrDepartment of Pathology, School of Medicine, Johns Hopkins University, Baltimore, Maryland, United States of America.ORCID http://orcid.org/0000-0002-6034-5962
Johns Hopkins University · USNational Heart Lung and Blood Institute · US

Funding

Traning Program in Environmental Health SciencesT32ES007141 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI Marsha Wills-Karp · 1985 to 2026
$22.2M
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
Mechanisms involved in male-female differences in cardioprotectionZIAHL002065 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI MURPHY, ELIZABETH · 2009 to 2025
$6.5M
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
Role of protein S-nitrosation in cardioprotectionF32HL096142 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI KOHR, MARK JEFFREY · 2009 to 2011
$144k
Intramural NIH HHS ZIA HL002065NHLBI NIH HHS F32 HL096142NHLBI NIH HHS K99 HL114721NHLBI NIH HHS R00 HL114721NHLBI NIH HHS R01 HL039752NIEHS NIH HHS T32 ES007141
6 · The paper itself

Abstract

Nitric oxide (NO) plays an important role in cardioprotection, and recent work from our group and others has implicated protein S-nitrosylation (SNO) as a critical component of NO-mediated protection in different models, including ischemic pre- and post-conditioning and sex-dependent cardioprotection. However, studies have yet to examine whether protein SNO levels are similarly increased with pharmacologic preconditioning in male and female hearts, and whether an increase in protein SNO levels, which is protective in male hearts, is sufficient to increase baseline protection in female hearts. Therefore, we pharmacologically preconditioned male and female hearts with the adenosine A1 receptor agonist N6-cyclohexyl adenosine (CHA). CHA administration prior to ischemia significantly improved functional recovery in both male and female hearts compared to baseline in a Langendorff-perfused heart model of ischemia-reperfusion injury (% of preischemic function ± SE: male baseline: 37.5±3.4% vs. male CHA: 55.3±3.2%; female baseline: 61.4±5.7% vs. female CHA: 76.0±6.2%). In a separate set of hearts, we found that CHA increased p-Akt and p-eNOS levels. We also used SNO-resin-assisted capture with LC-MS/MS to identify SNO proteins in male and female hearts, and determined that CHA perfusion induced a modest increase in protein SNO levels in both male (11.4%) and female (12.3%) hearts compared to baseline. These findings support a potential role for protein SNO in a model of pharmacologic preconditioning, and provide evidence to suggest that a modest increase in protein SNO levels is sufficient to protect both male and female hearts from ischemic injury. In addition, a number of the SNO proteins identified with CHA treatment were also observed with other forms of cardioprotective stimuli in prior studies, further supporting a role for protein SNO in cardioprotection.

Indexed as

AdenosineAdenosine A1 Receptor AgonistsAldehyde OxidoreductasesAnimalsCardiotonic AgentsFemaleMaleMice, Inbred C57BLMyocardial ContractionMyocardiumNitric Oxide Synthase Type IIIPerfusionPhosphorylationProto-Oncogene Proteins c-aktReactive Oxygen SpeciesReceptor, Adenosine A1AdenosineAdenosine A1 Receptor AgonistsAldehyde OxidoreductasesCardiotonic Agentsformaldehyde dehydrogenase, glutathione-independentN(6)-cyclohexyladenosineNitric Oxide Synthase Type IIIProto-Oncogene Proteins c-aktReactive Oxygen SpeciesReceptor, Adenosine A1S-Nitrosothiols

Identifiers

PMID28493997
PMCPMC5426678
OpenAlexW2612057859

What OpenQuestion holds

Textmetadata
LicenceCC0
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Registered trials

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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.