Evidence map›Paper›PMID 22989471›Full record

ArticleFree radical biology & medicine2013

Essential role of nitric oxide in acute ischemic preconditioning: S-nitros(yl)ation versus sGC/cGMP/PKG signaling?

Junhui Sun, Angel M Aponte, Mark J Kohr, Guang Tong, Charles Steenbergen, Elizabeth Murphy

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
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  13. Nitric Oxide Treatment for Lungs and Beyond. Novel Insights from Recent Literature.American journal of respiratory and critical care medicine · 2019
    Article
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  19. ProteinCirculation research · 2018
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Junhui SunSystems Biology Center, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA. sun1@mail.nih.gov
Angel M Aponte
Mark J Kohr
Guang Tong
Charles Steenbergen
Elizabeth Murphy
National Heart Lung and Blood Institute · USJohns Hopkins University · USNational Institutes of Health · USXijing Hospital · CN

Funding

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
Role of protein S-nitrosation in cardioprotectionF32HL096142 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI KOHR, MARK JEFFREY · 2009 to 2011
$144k
Intramural NIH HHS Z99 HL999999NHLBI NIH HHS 1F32HL096142NHLBI NIH HHS 5R01HL039752NHLBI NIH HHS F32 HL096142NHLBI NIH HHS K99 HL114721NHLBI NIH HHS R00 HL114721NHLBI NIH HHS R01 HL039752
6 · The paper itself

Abstract

Nitric oxide (NO) plays an important role in acute ischemic preconditioning (IPC). In addition to activating soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP)/protein kinase G (PKG) signaling pathways, NO-mediated protein S-nitros(yl)ation (SNO) has been recently shown to play an essential role in cardioprotection against ischemia-reperfusion (I/R) injury. In our previous studies, we have shown that IPC-induced cardioprotection could be blocked by treatment with either N-nitro-L-arginine methyl ester (L-NAME, a constitutive NO synthase inhibitor) or ascorbate (a reducing agent to decompose SNO). To clarify NO-mediated sGC/cGMP/PKG-dependent or -independent (i.e., SNO) signaling involved in IPC-induced cardioprotection, mouse hearts were Langendorff-perfused in the dark to prevent SNO decomposition by light exposure. Treatment with 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, a highly selective inhibitor of sGC) or KT5823 (a potent and selective inhibitor of PKG) did not abolish IPC-induced acute protection, suggesting that the sGC/cGMP/PKG signaling pathway does not play an important role in NO-mediated cardioprotective signaling during acute IPC. In addition, treatment with ODQ in IPC hearts provided an additional protective effect on functional recovery, in parallel with a higher SNO level in these ODQ+IPC hearts. In conclusion, these results suggest that the protective effect of NO is not related primarily to activation of the sGC/cGMP/PKG signaling pathway, but rather through SNO signaling in IPC-induced acute cardioprotection.

Indexed as

Ischemic Preconditioning, MyocardialAnimalsAscorbic AcidCarbazolesCells, CulturedCyclic GMP-Dependent Protein KinasesGuanylate CyclaseMaleMiceMice, Inbred C57BLMyocardiumNG-Nitroarginine Methyl EsterNitric OxideNitrosationOrgan Culture TechniquesOxadiazoles1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-oneAscorbic AcidCarbazolesCyclic GMP-Dependent Protein KinasesGuanylate CyclaseKT 5823NG-Nitroarginine Methyl EsterNitric OxideOxadiazolesQuinoxalines

Identifiers

PMID22989471
PMCPMC3539417
OpenAlexW2005539486

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.