Evidence map›Paper›PMID 38169612›Full record

ArticleInternational journal of biological sciences2024

METTL3 boosts mitochondrial fission and induces cardiac fibrosis after ischemia/reperfusion injury.

Li Ma, Xing Chang, Jing Gao, Ying Zhang, Ye Chen, Hao Zhou, Na Zhou, Na Du, Jiamin Li, Jiachen Bi and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of biological sciences, 2024. 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
3.8field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

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  11. Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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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

13 authors at 2 institutions in 1 country.

Li MaHeart Center, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Xing ChangGuang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China.
Jing GaoGuang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China.
Ying ZhangSenior Department of Cardiology, The Sixth Medical Center of People's Liberation Army General Hospital, Beijing 100048, China.
Ye ChenSenior Department of Cardiology, The Sixth Medical Center of People's Liberation Army General Hospital, Beijing 100048, China.
Hao ZhouSenior Department of Cardiology, The Sixth Medical Center of People's Liberation Army General Hospital, Beijing 100048, China.
Na ZhouHeart Center, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Na DuHeart Center, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Jiamin LiHeart Center, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Jiachen BiHeart Center, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Ziyue ChenHeart Center, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Xinxin ChenHeart Center, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Qingyong HeGuang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China.
Guangzhou Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

METTL3, an RNA methyltransferase enzyme, exerts therapeutic effects on various cardiovascular diseases. Myocardial ischemia-reperfusion injury (MIRI) and subsequently cardiac fibrosis is linked to acute cardiomyocyte death or dysfunction induced by mitochondrial damage, particularly mitochondrial fission. Our research aims to elucidate the potential mechanisms underlying the therapeutic actions of METTL3 in MIRI, with focus on mitochondrial fission. When compared with

Indexed as

Mitochondrial DynamicsMyocardial Reperfusion InjuryAnimalsApoptosisDNAFibrosisHumansIschemiaMethyltransferasesMiceMyocytes, CardiacDNAMethyltransferasesMETTL3 protein, humanMettl3 protein, mousecardiac ischemia-reperfusion injury.DNA-PKcsFis1METTL3mitochondrial fission

Identifiers

PMID38169612
PMCPMC10758110
OpenAlexW4389340114

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.