Evidence map›Paper›PMID 28662005›Full record

ArticleJournal of cardiovascular pharmacology2017

CaMKII Activation Promotes Cardiac Electrical Remodeling and Increases the Susceptibility to Arrhythmia Induction in High-fat Diet-Fed Mice With Hyperlipidemia Conditions.

Peng Zhong, Dajun Quan, Yan Huang, He Huang

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Journal of cardiovascular pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.0field-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

18 citing papers in PubMed, 37 citations in OpenAlex.

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  6. Neurogranin regulates calcium-dependent cardiac hypertrophy.Experimental and molecular pathology · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Peng Zhong*Department of Cardiology, Renming Hospital of Wuhan University, Wuhan, PR China; †Cardiovascular Research Institute, Wuhan University, Wuhan, PR China; and ‡Huei Key Laboratory of Cardiology, Wuhan, PR China.
Dajun Quan
Yan Huang
He Huang
Renmin Hospital of Wuhan University · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundObesity/hyperlipidemia is closely related to both atrial and ventricular arrhythmias. CaMKII, a multifunctional serine/threonine kinase, has been involved in cardiac arrhythmias of different etiologies. However, its role in obesity/hyperlipidemia-related cardiac arrhythmia is unexplored. The aim of this was to determine the involvement of CaMKII in the process.

methodsAdult male APOE mice were fed a high-fat diet (HFD), administrated with KN93 (10 mg·kg·2d), a specific inhibitor of CaMKII. Serum lipid and glucose profile, cardiac function, and surface electrocardiogram were determined. Electrophysiological study and epicardial activation mapping were performed in Langendorff-perfused heart. Expression of cardiac ion channels, gap junction proteins, Ca handling proteins, and CaMKII were evaluated, coupled with histological analysis.

resultsA hyperlipidemia condition was induced by HFD in the APOE mice, which was associated with increased expression and activity of CaMKII in the hearts. In Langendorff-perfused hearts, HFD-induced heart showed increased arrhythmia inducibility, prolonged action potential duration, and decreased action potential duration alternans thresholds, coupled with slow ventricular conduction, connexin-43 upregulation, and interstitial fibrosis. Downregulation of ion channels including Cav1.2 and Kv4.2/Kv4.3 and disturbed Ca handling proteins were also observed in HFD-induced heart. Interestingly, all these alterations were significantly inhibited by KN93 treatment.

conclusionOur results demonstrated an adverse effect of metabolic components on cardiac electrophysiology and implicated an important role of CaMKII underlying this process.

Indexed as

AnimalsArrhythmias, CardiacAtrial RemodelingCalcium-Calmodulin-Dependent Protein Kinase Type 2Diet, High-FatEnzyme ActivationHyperlipidemiasIsolated Heart PreparationMaleMiceMice, Inbred C57BLMice, KnockoutCalcium-Calmodulin-Dependent Protein Kinase Type 2

Identifiers

PMID28662005
PMCPMC5642343
OpenAlexW2731687733

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.