Evidence map›Paper›PMID 27186301›Full record

ArticleAmerican journal of translational research2016

Cardiomyocyte specific deletion of PP2A causes cardiac hypertrophy.

Lei Li, Chao Fang, Di Xu, Yidan Xu, Heling Fu, Jianmin Li

Abstract read
In one paragraph

Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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.

  1. Article
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  4. Article
  5. Article
  6. The role of β-catenin in cardiac diseases.Frontiers in pharmacology · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Roles and regulation of protein phosphatase 2A (PP2A) in the heart.Journal of molecular and cellular cardiology · 2016
    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.

Lei LiDepartment of Pharmacology, Basic Medical Sciences of Nanjing Medical University Nanjing 210029, Jiangsu, China.
Chao FangDepartment of Pharmacology, Basic Medical Sciences of Nanjing Medical University Nanjing 210029, Jiangsu, China.
Di XuNanjing Medical University Nanjing 210029, Jiangsu, China.
Yidan XuDepartment of Ophthalmology, The First Affiliated Hospital of Nanjing Medical University Nanjing 210029, Jiangsu, China.
Heling FuModel Animal Research Center of Nanjing Medical University Nanjing, Jiangsu 210029, China.
Jianmin LiDepartment of Pharmacology, Basic Medical Sciences of Nanjing Medical University Nanjing 210029, Jiangsu, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac hypertrophy is a common pathological alteration in heart disease, which has been reported to be connected with serine/threonine protein phosphatases that control the dephosphorylation of a variety of cardiac proteins. Herein, we generated protein phosphatase type 2A knockout expressing a tamoxifen-inducible Cre recombinase protein fused to two mutant estrogen-receptor ligand-binding domains (MerCreMer) under the control of the a-myosin heavy chain promoter. Cardiac function of mice was determined by echocardiography. Decrease in PP2A activity leads to increased cardiomyocyte hypertrophy and fibrosis. Loss of PP2ACα leads to the heart failure, including the changes of EF, FS, LV, ANP and BNP. On the molecular level, knockout mice shows increased expression of B55a and B56e at 60 days after tamoxifen injection. Additionally, the regulation of the Akt/GSK3β/β-catenin pathway is severely disturbed in knockout mice. In conclusion, cardiomyocyte specific deletion of PP2A gene causes the cardiac hypertrophy. We will use the knockout mice to generate a type of cardiomyocyte hypertrophy mouse model with myocardial fibrosis.

Indexed as

hypertrophyknockout mouse modelPP2A

Identifiers

PMID27186301
PMCPMC4859906

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.