Evidence map›Paper›PMID 33452765›Full record

ArticleJournal of cellular and molecular medicine2021

Knockout of MYOM1 in human cardiomyocytes leads to myocardial atrophy via impairing calcium homeostasis.

Chengwen Hang, Yuanxiu Song, Ya'nan Li, Siyao Zhang, Yun Chang, Rui Bai, Amina Saleem, Mengqi Jiang, Wenjing Lu, Feng Lan and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

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  5. CTCF Mediates the Cis-Regulatory Hubs in Mouse Hearts.International journal of molecular sciences · 2025
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  20. Evolutionary context of psoriatic immune skin response.Evolution, medicine, and public health · 2021
    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

11 authors at 2 institutions in 1 country.

Chengwen HangDepartment of Cardiology, Peking University Third Hospital, Beijing, China.
Yuanxiu SongDepartment of Cardiology, Peking University Third Hospital, Beijing, China.
Ya'nan LiBeijing Lab for Cardiovascular Precision Medicine, Anzhen Hospital, Capital Medical University, Beijing, China.
Siyao ZhangBeijing Lab for Cardiovascular Precision Medicine, Anzhen Hospital, Capital Medical University, Beijing, China.
Yun ChangBeijing Lab for Cardiovascular Precision Medicine, Anzhen Hospital, Capital Medical University, Beijing, China.
Rui BaiBeijing Lab for Cardiovascular Precision Medicine, Anzhen Hospital, Capital Medical University, Beijing, China.
Amina SaleemBeijing Lab for Cardiovascular Precision Medicine, Anzhen Hospital, Capital Medical University, Beijing, China.
Mengqi JiangDepartment of Cardiology, Peking University Third Hospital, Beijing, China.
Wenjing LuBeijing Lab for Cardiovascular Precision Medicine, Anzhen Hospital, Capital Medical University, Beijing, China.
Feng LanBeijing Lab for Cardiovascular Precision Medicine, Anzhen Hospital, Capital Medical University, Beijing, China.ORCID 0000-0002-9038-4014
Ming CuiDepartment of Cardiology, Peking University Third Hospital, Beijing, China.
Capital Medical University · CNPeking University · CN

Funding

National Natural Science Foundation of China 81570215National Natural Science Foundation of China 81570235National Natural Science Foundation of China 81970205National Natural Science Foundation of China 82070272Natural Science Foundation of Beijing Municipality 7202225Natural Science Foundation of Beijing Municipality Z190013
6 · The paper itself

Abstract

Myomesin-1 (encoded by MYOM1 gene) is expressed in almost all cross-striated muscles, whose family (together with myomesin-2 and myomesin-3) helps to cross-link adjacent myosin to form the M-line in myofibrils. However, little is known about its biological function, causal relationship and mechanisms underlying the MYOM1-related myopathies (especially in the heart). Regrettably, there is no MYMO1 knockout model for its study so far. A better and further understanding of MYOM1 biology is urgently needed. Here, we used CRISPR/Cas9 gene-editing technology to establish an MYOM1 knockout human embryonic stem cell line (MYOM1

Indexed as

Disease SusceptibilityAllelesCalciumCell DifferentiationCell LineConnectinEmbryonic Stem CellsGene EditingGene Expression ProfilingGene Knockout TechniquesGenetic Predisposition to DiseaseHumansMolecular ImagingMuscular AtrophyMyocytes, CardiacPhenotypeCalciumConnectinMYOM1 protein, humancalcium homeostasisCaMKIIhESC-CMsmyocardial atrophymyocardial contractionMYOM1 knockoutmyomesin-1 deficiency

Identifiers

PMID33452765
PMCPMC7875908
OpenAlexW3125436700

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.