Evidence map›Paper›PMID 30005556›Full record

ArticleJournal of the American Heart Association2018

Gastrin Protects Against Myocardial Ischemia/Reperfusion Injury via Activation of RISK (Reperfusion Injury Salvage Kinase) and SAFE (Survivor Activating Factor Enhancement) Pathways.

Xiaoli Yang, Rongchuan Yue, Jun Zhang, Xiaoqun Zhang, Yukai Liu, Caiyu Chen, Xinquan Wang, Hao Luo, Wei Eric Wang, Xiongwen Chen and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.5field-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

15 citing papers in PubMed, 32 citations in OpenAlex.

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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

14 authors at 4 institutions in 2 countries.

Xiaoli YangDepartment of Cardiology, Chongqing Institute of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, China.
Rongchuan YueDepartment of Cardiology, North Sichuan Medical College First Affiliated Hospital, Nanchong, Sichuan, China.
Jun ZhangDepartment of Cardiology, Chongqing Institute of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, China.
Xiaoqun ZhangDepartment of Cardiology, Chongqing Institute of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, China.
Yukai LiuDepartment of Cardiology, Chongqing Institute of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, China.
Caiyu ChenDepartment of Cardiology, Chongqing Institute of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, China.
Xinquan WangDepartment of Cardiology, Chongqing Institute of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, China.
Hao LuoDepartment of Cardiology, Chongqing Institute of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, China.
Wei Eric WangDepartment of Cardiology, Chongqing Institute of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, China.
Xiongwen ChenDepartment of Cardiology, Chongqing Institute of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, China.
Huixia Judy WangDepartment of Statistics, The George Washington University, Washington, DC.
Pedro A JoseDivision of Renal Disease & Hypertension, The George Washington University School of Medicine & Health Sciences, Washington, DC.
Hongyong WangDepartment of Cardiology, Chongqing Institute of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, China chunyuzeng01@163.com whysir@aliyun.com.
Chunyu ZengDepartment of Cardiology, Chongqing Institute of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, China chunyuzeng01@163.com whysir@aliyun.com.
Daping Hospital · CNArmy Medical University · CNGeorge Washington University · USNorth Sichuan Medical University · CN

Funding

Spatiotemporal transregulation of D1-like angiotensin receptors in genetically...P01HL074940 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI GILDEA, JOHN JOSEPH · 2004 to 2020
$31.8M
RENAL DOPAMINE-1 RECEPTOR DEFECT IN HYPERTENSIONR01DK039308 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI JOSE, PEDRO A. · 1987 to 2020
$7.4M
Renal Dopamine Receptor & RegulationR37HL023081 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI JOSE, PEDRO A. · 2007 to 2016
$4.3M
RENAL DOPAMINE RECEPTOR REGULATION AND FUNCTIONR01HL023081 · NHLBI · GEORGETOWN UNIVERSITY · PI JOSE, PEDRO A. · 1985 to 2006
$2.4M
NHLBI NIH HHS P01 HL074940NHLBI NIH HHS R01 HL023081NHLBI NIH HHS R37 HL023081NIDDK NIH HHS R01 DK039308
6 · The paper itself

Abstract

backgroundIschemia/reperfusion injury (IRI) is one of the most predominant complications of ischemic heart disease. Gastrin has emerged as a regulator of cardiovascular function, playing a key protective role in hypoxia. Serum gastrin levels are increased in patients with myocardial infarction, but the pathophysiogical significance of this finding is unknown. The purpose of this study was to determine whether and how gastrin protects cardiac myocytes from IRI. METHODS AND

resultsAdult male Sprague-Dawley rats were used in the experiments. The hearts in living rats or isolated Langendorff-perfused rat hearts were subjected to ischemia followed by reperfusion to induce myocardial IRI. Gastrin, alone or with an antagonist, was administered before the induction of myocardial IRI. We found that gastrin improved myocardial function and reduced the expression of myocardial injury markers, infarct size, and cardiomyocyte apoptosis induced by IRI. Gastrin increased the phosphorylation levels of ERK1/2 (extracellular signal-regulated kinase 1/2), AKT (protein kinase B), and STAT3 (signal transducer and activator of transcription 3), indicating its ability to activate the RISK (reperfusion injury salvage kinase) and SAFE (survivor activating factor enhancement) pathways. The presence of inhibitors of ERK1/2, AKT, or STAT3 abrogated the gastrin-mediated protection. The protective effect of gastrin was via CCK2R (cholecystokinin 2 receptor) because the CCK2R blocker CI988 prevented the gastrin-mediated protection of the heart with IRI. Moreover, we found a negative correlation between serum levels of cardiac troponin I and gastrin in patients with unstable angina pectoris undergoing percutaneous coronary intervention, suggesting a protective effect of gastrin in human cardiomyocytes.

conclusionsThese results indicate that gastrin can reduce myocardial IRI by activation of the RISK and SAFE pathways.

Indexed as

AgedAngina, UnstableAnimalsApoptosisFemaleGastrinsHeartHormonesHumansIsolated Heart PreparationMaleMAP Kinase Signaling SystemMiddle AgedMyocardial InfarctionMyocardial Reperfusion InjuryMyocardiumGastrinsHormonesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktReceptor, Cholecystokinin BStat3 protein, ratSTAT3 Transcription FactorTroponin Igastrinischemia/reperfusion injuryLangendorffreperfusion injury salvage kinaseRISK (reperfusion injury salvage kinase)SAFE (survivor activating factor enhancement)

Identifiers

PMID30005556
PMCPMC6064830
OpenAlexW2811619697

What OpenQuestion holds

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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.