Evidence map›Paper›PMID 20833954›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2010

Calcium-sensing receptor: a sensor and mediator of ischemic preconditioning in the heart.

Junhui Sun, Elizabeth Murphy

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.4field-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

24 citing papers in PubMed, 53 citations in OpenAlex.

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  18. Cardioprotective Role of Caveolae in Ischemia-Reperfusion Injury.Translational medicine (Sunnyvale, Calif.) · 2013
    Article
  19. Article
  20. Regulation of ca(2+) signaling in pulmonary hypertension.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2013
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Junhui SunTranslational Medicine Branch, National Heart Lung and Blood Institute, National Institutes of Health, Bldg 10/Rm 8N206, Bethesda, MD 20892,USA. sun1@mail.nih.gov
Elizabeth Murphy
National Heart Lung and Blood Institute · USNational Institutes of Health · 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
Intramural NIH HHS
6 · The paper itself

Abstract

As a G protein-coupled receptor, the extracellular Ca(2+)-sensing receptor (CaSR) responds to changes not only in extracellular Ca(2+), but also to many other ligands. CaSR has been found to be expressed in the hearts and cardiovascular system. In this study, we confirmed that CaSR is expressed in mouse cardiomyocytes and showed that it is predominantly localized in caveolae. The goal of this study was to investigate whether CaSR plays a cardioprotective role in ischemic preconditioning (IPC). Hearts from C57BL/6J mice (male, 12-16 wk) were perfused in the Langendorff mode and subjected to the following treatments: 1) control perfusion; 2) perfusion with a specific CaSR antagonist, NPS2143; 3) IPC (four cycles of 5 min of global ischemia and 5 min of reperfusion); or 4) perfusion with NPS2143 before and during IPC. Following these treatments, hearts were subjected to 20 min of no-flow global ischemia and 120 min of reperfusion. Compared with control, IPC significantly improved postischemic left ventricular functional recovery and reduced infarct size. Although NPS2143 perfusion alone did not change the hemodynamic function and did not change the extent of postischemic injury, NPS2143 treatment abolished cardioprotection of IPC. Through immunoblot analysis, it was demonstrated that IPC significantly increased the levels of phosphorylated ERK1/2, AKT, and GSK-3β, which were also prevented by NPS2143 treatment. Taken together, the distribution of CaSR in caveolae along with NPS2143-blockade of IPC-induced cardioprotective signaling suggest that the activation of CaSR during IPC is cardioprotective by a process involving caveolae.

Indexed as

Ischemic Preconditioning, MyocardialAnimalsCaveolin 3Extracellular Signal-Regulated MAP KinasesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaMaleMiceMice, Inbred C57BLModels, AnimalMyocardial Reperfusion InjuryMyocytes, CardiacNaphthalenesParathyroid Hormone-Related ProteinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCav3 protein, mouseCaveolin 3Extracellular Signal-Regulated MAP KinasesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, mouseN-(2-hydroxy-3-(2-cyano-3-chlorophenoxy)propyl)-1,1-dimethyl-2-(2-nephthyl)ethylamineNaphthalenesParathyroid Hormone-Related ProteinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Calcium-Sensing

Identifiers

PMID20833954
PMCPMC2993222
OpenAlexW2102687692

What OpenQuestion holds

Textmetadata
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.