Evidence map›Paper›PMID 35433671›Full record

ArticleFrontiers in cell and developmental biology2022

Cas9/AAV9-Mediated Somatic Mutagenesis Uncovered the Cell-Autonomous Role of Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase 2 in Murine Cardiomyocyte Maturation.

Junsen Lin, Zhan Chen, Luzi Yang, Lei Liu, Peng Yue, Yueshen Sun, Mingming Zhao, Xiaoling Guo, Xiaomin Hu, Yan Zhang and 4 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

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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

14 authors at 5 institutions in 1 country.

Junsen LinPeking University Health Science Center, School of Basic Medical Sciences, The Institute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Science of Ministry of Education, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing, China.
Zhan ChenPeking University Health Science Center, School of Basic Medical Sciences, The Institute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Science of Ministry of Education, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing, China.
Luzi YangPeking University Health Science Center, School of Basic Medical Sciences, The Institute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Science of Ministry of Education, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing, China.
Lei LiuKey Laboratory of Birth Defects and Related Diseases of Women and Children of Ministry of Education (MOE), Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, China.
Peng YueKey Laboratory of Birth Defects and Related Diseases of Women and Children of Ministry of Education (MOE), Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, China.
Yueshen SunState Key Laboratory of Complex Severe and Rare Diseases, Department of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China.
Mingming ZhaoDepartment of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission of China (NHC) Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research. Beijing, China.
Xiaoling GuoBasic Medical Research Center, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.
Xiaomin HuState Key Laboratory of Complex Severe and Rare Diseases, Department of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China.
Yan ZhangPeking University Health Science Center, School of Basic Medical Sciences, The Institute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Science of Ministry of Education, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing, China.
Hong ZhangPeking University Health Science Center, School of Basic Medical Sciences, The Institute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Science of Ministry of Education, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing, China.
Yifei LiKey Laboratory of Birth Defects and Related Diseases of Women and Children of Ministry of Education (MOE), Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, China.
Yuxuan GuoPeking University Health Science Center, School of Basic Medical Sciences, The Institute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Science of Ministry of Education, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing, China.
Erdan DongPeking University Health Science Center, School of Basic Medical Sciences, The Institute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Science of Ministry of Education, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing, China.
Peking University · CNSichuan University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNPeking University Third Hospital · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sarcoplasmic/endoplasmic reticulum calcium ATPase 2 (SERCA2) is a key player in cardiomyocyte calcium handling and also a classic target in the gene therapy for heart failure. SERCA2 expression dramatically increases during cardiomyocyte maturation in the postnatal phase of heart development, which is essential for the heart to acquire its full function in adults. However, whether and how SERCA2 regulates cardiomyocyte maturation remains unclear. Here, we performed Cas9/AAV9-mediated somatic mutagenesis (CASAAV) in mice and achieved cardiomyocyte-specific knockout of

Indexed as

cardiomyocyte maturationCas9/AAV9-mediated somatic mutagenesisgenetic mosaic analysisheart failuresarcoplasmic/endoplasmic reticulum calcium ATPase 2

Identifiers

PMID35433671
PMCPMC9012521
OpenAlexW4220732514

What OpenQuestion holds

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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.