Evidence map›Paper›PMID 32207065›Full record

ArticleScience China. Life sciences2020

MYH7B variants cause hypertrophic cardiomyopathy by activating the CaMK-signaling pathway.

Peng Chen, Zongzhe Li, Jiali Nie, Hong Wang, Bo Yu, Zheng Wen, Yang Sun, Xiaolu Shi, Li Jin, Dao-Wen Wang

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Science China. Life sciences, 2020. 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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 32 citations in OpenAlex.

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  14. Circulating miR-499a-5p Is a Potential Biomarker ofInternational journal of molecular sciences · 2022
    Article
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  17. Transcriptional regulation of intermolecular CaProceedings of the National Academy of Sciences of the United States of America · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Peng ChenDivision of Cardiology, Departments of Internal Medicine and Genetic Diagnosis Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Zongzhe LiDivision of Cardiology, Departments of Internal Medicine and Genetic Diagnosis Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Jiali NieDivision of Cardiology, Departments of Internal Medicine and Genetic Diagnosis Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Hong WangDivision of Cardiology, Departments of Internal Medicine and Genetic Diagnosis Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Bo YuDivision of Cardiology, Departments of Internal Medicine and Genetic Diagnosis Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Zheng WenDivision of Cardiology, Departments of Internal Medicine and Genetic Diagnosis Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Yang SunDivision of Cardiology, Departments of Internal Medicine and Genetic Diagnosis Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Xiaolu ShiExperimental Research Center, China Academy of Chinese Medical Sciences, Beijing, 100700, China.
Li JinDivision of Cardiology, Departments of Internal Medicine and Genetic Diagnosis Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Dao-Wen WangDivision of Cardiology, Departments of Internal Medicine and Genetic Diagnosis Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. dwwang@tjh.tjmu.edu.cn.
Huazhong University of Science and Technology · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNTongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertrophic cardiomyopathy (HCM) is a common genetic disease, predominantly caused by mutations in cardiac sarcomere genes; however, whether MYH7B causes HCM is not known. In this study, 549 unrelated patients with HCM and 500 healthy-controls were screened using targeted sequencing and whole exome sequencing together. We observed seven variants in MYH7B causing HCM in 8/549 patients, which accounted for 1.46% of HCM cases. Of these seven variants, three likely pathogenic variants in MYH7B co-segregating with 5 HCM patients were identified in three HCM pedigrees without other HCM-associated variants. Myh7b knockout rats were generated and cardiac functions were detected by Millar pressure-volume catheterization and echocardiography. Spontaneous HCM phenotypes, cellular disarray and cardiac fibrosis were observed in both Myh7b

Indexed as

AgedAnimalsCalcium-Calmodulin-Dependent Protein KinasesCardiac MyosinsCardiomyopathy, HypertrophicCohort StudiesExome SequencingFemaleGene Expression RegulationGene Knockout TechniquesHeartHumansMaleMicroRNAsMiddle AgedMutant ProteinsCalcium-Calmodulin-Dependent Protein KinasesCardiac MyosinsMicroRNAsMIRN208 microRNA, humanMIRN499 microRNA, humanMutant ProteinsMYH7 protein, humanMyosin Heavy ChainsCaMK-signaling pathwayhypertrophic cardiomyopathyMYH7Btranscriptome sequencingwhole exome sequencing

Identifiers

PMID32207065
OpenAlexW3012866509

What OpenQuestion holds

Textmetadata
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.