Evidence map›Paper›PMID 39536197›Full record

ArticleArquivos brasileiros de cardiologia2024

LncRNA CCAT2 Knockdown Alleviates Pressure Overload or Ang II-Induced Cardiac Hypertrophy Via Disruption of the Wnt/β-Catenin Signaling.

Xiaojun Zhang, Zhen Chen, Ning Zhang, Bo Yu, Wei Li, Mengli Zhang, Xian Wu, Ganzhe Liu, Meizhen Dong

Abstract read
In one paragraph

Article in Arquivos brasileiros de cardiologia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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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

2 citing papers in PubMed.

  1. Review
  2. Long Non-Coding RNA CCAT2 and Pathological Cardiac Remodeling.Arquivos brasileiros de cardiologia · 2024
    Article
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

9 authors.

Xiaojun ZhangDepartment of Emergency, Qilu Hospital (Qingdao), Cheeloo College of Medicine, Shangdong University, Qingdao, Shangdong - China.
Zhen ChenThe Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei - China.
Ning ZhangDepartment of Emergency, Qilu Hospital (Qingdao), Cheeloo College of Medicine, Shangdong University, Qingdao, Shangdong - China.
Bo YuThe Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei - China.
Wei LiThe Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei - China.
Mengli ZhangThe Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei - China.
Xian WuThe Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei - China.
Ganzhe LiuThe Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei - China.
Meizhen DongDepartment of Emergency, Qilu Hospital (Qingdao), Cheeloo College of Medicine, Shangdong University, Qingdao, Shangdong - China.ORCID 0009-0007-0938-9584

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSustained pathological cardiac hypertrophy (CH) is an independent risk factor for increased incidence and mortality of cardiovascular events.

objectivesThis research was designed to unravel the role of long non-coding RNA (LncRNA) CCAT2 in CH progression.

methodsTransverse aortic constriction (TAC) procedures were conducted to construct a pressure overload-induced in vivo CH model. Angiotensin II (Ang II) treatment was utilized to induce hypertrophic rat cardiomyocyte H9c2 cells.

resultsIn vivo results showed that silencing of CCAT2 reduced cardiomyocyte surface area, alleviated cardiac fibrosis, and decreased β-MHC, ANP, and BNP levels in CH mouse models. In vitro results revealed that CCAT2 knockdown reduced cell surface area and attenuated β-MHC, ANP, and BNP levels in hypertrophic H9c2 cells. Besides, CCAT2 silencing decreased the levels of active β-catenin, phosphorylated-GSK-3β, and Wnt target genes (c-Myc, cyclinD1, and c-Jun) in CH mice and hypertrophic H9c2 cells. Importantly, treatment with the Wnt/β-catenin pathway activator LiCl reversed the suppression of CCAT2 knockdown on H9c2 cell surface area and MHC, ANP, and BNP levels.

conclusionsCollectively, CCAT2 silencing plays a protective role against CH through inactivating the Wnt/β-catenin signaling, which suggests that CCAT2 might become a promising therapeutic target for CH.

Indexed as

Angiotensin IICardiomegalyDisease Models, AnimalRNA, Long NoncodingWnt Signaling PathwayAnimalsbeta CateninGene Knockdown TechniquesMaleMiceMice, Inbred C57BLMyocytes, CardiacRatsAngiotensin IIbeta CateninRNA, Long Noncoding

Identifiers

PMID39536197
PMCPMC11634213

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LicenceCC BY
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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.