Evidence map›Paper›PMID 40346382›Full record

ArticleCommunications biology2025

Krüppel like factor 7 regulates mitochondrial dynamics balance in myocardial infarction.

Cao Wang, Fuxing Zhu, Lan Zhou, Situo Zhang, Ruiqi Wang, Hui Tian, Bosong Zhang, Jiahui Wu, Xiang Xu, Ruixian Jiang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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

1 citing paper in PubMed.

  1. Review
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.

Cao Wang *School of Life Science and Technology, Harbin Institute of Technology, Harbin, 150080, China.
Fuxing Zhu *School of Life Science and Technology, Harbin Institute of Technology, Harbin, 150080, China.
Lan ZhouThe Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, 150001, China, Harbin.
Situo ZhangSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, 150080, China.
Ruiqi WangSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, 150080, China.
Hui TianSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, 150080, China.
Bosong ZhangSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, 150080, China.
Jiahui WuSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, 150080, China.
Xiang XuSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, 150080, China.
Ruixian JiangSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, 150080, China.
Xiaolu HouDepartment of Cardiology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, 150081, China.
Jian LiuSchool of Instrumentation Science and Engineering, Harbin Institute of Technology, Harbin, 150080, China.
Weiming TianSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, 150080, China. tianweiming@hit.edu.cn.ORCID http://orcid.org/0000-0003-4958-4118

Funding

China Postdoctoral Science Foundation 2024M764164Heilongjiang Postdoctoral Science Foundation LBH-Z24017National Natural Science Foundation of China (National Science Foundation of China) 82400320Postdoctoral Research Foundation of China (China Postdoctoral Research Foundation) GZC20242212
6 · The paper itself

Abstract

Targeting the balance of mitochondrial fission and fusion can effectively alleviate the cardiac energy supply efficiency, to restore cardiac systolic dysfunction and reduce mortality. We previously found that Klf7 is closely related to cardiac energy metabolism. Here we generated cardiomyocyte-specific Klf7 knockout and overexpression mice that underwent myocardial infarction (MI) surgery. Klf7 expression increased in the ischemic myocardium of mice, and cardiomyocyte-specific knockout Klf7 significantly lowered the mortality of MI-inflicted mice and improved ATP insufficiency in MI. Subsequently, Klf7 overexpression aggravated adverse cardiac remodeling and mitochondrial fission and fusion imbalance after MI. Our results also demonstrated that Klf7 inhibited mitochondrial fusion and promoted mitochondrial fission by targeting prohibitin 2 (Phb2) and mitofusin 2 (Mfn2). Our study revealed a crucial role in upholding the overall balance of mitochondrial fission and fusion during MI. Furthermore, our findings indicated that the Klf7/Mfn2/Phb2 axis holds promise as a potential target for therapeutic interventions of MI.

Indexed as

Kruppel-Like Transcription FactorsMitochondrial DynamicsMyocardial InfarctionAnimalsGTP PhosphohydrolasesMaleMiceMice, Inbred C57BLMice, KnockoutMitochondrial ProteinsMyocytes, CardiacProhibitinsRepressor ProteinsGTP PhosphohydrolasesKlf7 protein, mouseKruppel-Like Transcription FactorsMfn2 protein, mouseMitochondrial ProteinsPhb2 protein, mouseProhibitinsRepressor Proteins

Identifiers

PMID40346382
PMCPMC12064834

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.