Evidence map›Paper›PMID 26882027›Full record

ArticlePloS one2016

Alk7 Depleted Mice Exhibit Prolonged Cardiac Repolarization and Are Predisposed to Ventricular Arrhythmia.

Shaozhen Ying, Hong Cao, He Hu, Xin Wang, Yanhong Tang, Congxin Huang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. KCells · 2023
    Review
  3. Article
  4. Modeling the human heart ex vivo-current possibilities and strive for future applications.Journal of tissue engineering and regenerative medicine · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
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 1 country.

Shaozhen YingDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China, 238 Jiefang Road, Wuchang District, Wuhan 430060, Hubei Province, China.
Hong CaoDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China, 238 Jiefang Road, Wuchang District, Wuhan 430060, Hubei Province, China.
He HuDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China, 238 Jiefang Road, Wuchang District, Wuhan 430060, Hubei Province, China.
Xin WangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China, 238 Jiefang Road, Wuchang District, Wuhan 430060, Hubei Province, China.
Yanhong TangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China, 238 Jiefang Road, Wuchang District, Wuhan 430060, Hubei Province, China.
Congxin HuangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China, 238 Jiefang Road, Wuchang District, Wuhan 430060, Hubei Province, China.
Wuhan University · CNRenmin Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We aimed to investigate the role of activin receptor-like kinase (ALK7) in regulating cardiac electrophysiology. Here, we showed that Alk7-/- mice exhibited prolonged QT intervals in telemetry ECG recordings. Furthermore, Langendorff-perfused Alk7-/- hearts had significantly longer action potential duration (APD) and greater incidence of ventricular arrhythmia (AV) induced by burst pacing. Using whole-cell patch clamp, we found that the densities of repolarizing K+ currents Ito and IK1 were profoundly reduced in Alk7-/- ventricular cardiomyocytes. Mechanistically, the expression of Kv4.2 (a major subunit of Ito carrying channel) and KCHIP2 (a key accessory subunit of Ito carrying channel), was markedly decreased in Alk7-/- hearts. These findings suggest that endogenous expression of ALK7 is necessary to maintain repolarizing K+ currents in ventricular cardiomyocytes, and finally prevent action potential prolongation and ventricular arrhythmia.

Indexed as

Action PotentialsActivin Receptors, Type IAnimalsArrhythmias, CardiacCell SeparationDisease SusceptibilityElectrocardiographyHeart VentriclesIn Vitro TechniquesMice, Inbred C57BLMyocytes, CardiacPerfusionPotassium Channels, Tandem Pore DomainProtein SubunitsTelemetryUltrasonographyActivin Receptors, Type IAcvr1c protein, mousePotassium Channels, Tandem Pore DomainProtein Subunits

Identifiers

PMID26882027
PMCPMC4755580
OpenAlexW2280211126

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.