Evidence map›Paper›PMID 24763737›Full record

ArticlePloS one2014

Never in mitosis gene A related kinase-6 attenuates pressure overload-induced activation of the protein kinase B pathway and cardiac hypertrophy.

Zhouyan Bian, Haihan Liao, Yan Zhang, Qingqing Wu, Heng Zhou, Zheng Yang, Jinrong Fu, Teng Wang, Ling Yan, Difei Shen and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  9. Mitotic Regulation by NEK Kinase Networks.Frontiers in cell and developmental biology · 2017
    Review
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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

12 authors at 2 institutions in 1 country.

Zhouyan BianDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, P. R. China; Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei Province, P. R. China.
Haihan LiaoDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, P. R. China; Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei Province, P. R. China.
Yan ZhangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, P. R. China; Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei Province, P. R. China.
Qingqing WuDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, P. R. China; Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei Province, P. R. China.
Heng ZhouDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, P. R. China.
Zheng YangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, P. R. China; Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei Province, P. R. China.
Jinrong FuDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, P. R. China.
Teng WangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, P. R. China; Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei Province, P. R. China.
Ling YanDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, P. R. China.
Difei ShenDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, P. R. China.
Hongliang LiDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, P. R. China; Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei Province, P. R. China.
Qizhu TangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, P. R. China; Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei Province, P. R. China.
Renmin Hospital of Wuhan University · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac hypertrophy appears to be a specialized form of cellular growth that involves the proliferation control and cell cycle regulation. NIMA (never in mitosis, gene A)-related kinase-6 (Nek6) is a cell cycle regulatory gene that could induce centriole duplication, and control cell proliferation and survival. However, the exact effect of Nek6 on cardiac hypertrophy has not yet been reported. In the present study, the loss- and gain-of-function experiments were performed in Nek6 gene-deficient (Nek6-/-) mice and Nek6 overexpressing H9c2 cells to clarify whether Nek6 which promotes the cell cycle also mediates cardiac hypertrophy. Cardiac hypertrophy was induced by transthoracic aorta constriction (TAC) and then evaluated by echocardiography, pathological and molecular analyses in vivo. We got novel findings that the absence of Nek6 promoted cardiac hypertrophy, fibrosis and cardiac dysfunction, which were accompanied by a significant activation of the protein kinase B (Akt) signaling in an experimental model of TAC. Consistent with this, the overexpression of Nek6 prevented hypertrophy in H9c2 cells induced by angiotonin II and inhibited Akt signaling in vitro. In conclusion, our results demonstrate that the cell cycle regulatory gene Nek6 is also a critical signaling molecule that helps prevent cardiac hypertrophy and inhibits the Akt signaling pathway.

Indexed as

MitosisAnimalsCardiomegalyCells, CulturedHumansMaleMiceMice, KnockoutMuscle CellsNIMA-Related KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktSignal TransductionNEK6 protein, humanNIMA-Related KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID24763737
PMCPMC3999101
OpenAlexW1998395515

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.