Krüppel like factor 7 regulates mitochondrial dynamics balance in myocardial infarction

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 cardiomyoc...

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Main Authors: Cao Wang, Fuxing Zhu, Lan Zhou, Situo Zhang, Ruiqi Wang, Hui Tian, Bosong Zhang, Jiahui Wu, Xiang Xu, Ruixian Jiang, Xiaolu Hou, Jian Liu, Weiming Tian
Format: Article
Language:English
Published: Nature Portfolio 2025-05-01
Series:Communications Biology
Online Access:https://doi.org/10.1038/s42003-025-08139-z
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author Cao Wang
Fuxing Zhu
Lan Zhou
Situo Zhang
Ruiqi Wang
Hui Tian
Bosong Zhang
Jiahui Wu
Xiang Xu
Ruixian Jiang
Xiaolu Hou
Jian Liu
Weiming Tian
author_facet Cao Wang
Fuxing Zhu
Lan Zhou
Situo Zhang
Ruiqi Wang
Hui Tian
Bosong Zhang
Jiahui Wu
Xiang Xu
Ruixian Jiang
Xiaolu Hou
Jian Liu
Weiming Tian
author_sort Cao Wang
collection DOAJ
description 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.
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institution Kabale University
issn 2399-3642
language English
publishDate 2025-05-01
publisher Nature Portfolio
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series Communications Biology
spelling doaj-art-7cf707f8c01f46b68a4ed370c81de7682025-08-20T03:52:55ZengNature PortfolioCommunications Biology2399-36422025-05-018111610.1038/s42003-025-08139-zKrüppel like factor 7 regulates mitochondrial dynamics balance in myocardial infarctionCao Wang0Fuxing Zhu1Lan Zhou2Situo Zhang3Ruiqi Wang4Hui Tian5Bosong Zhang6Jiahui Wu7Xiang Xu8Ruixian Jiang9Xiaolu Hou10Jian Liu11Weiming Tian12School of Life Science and Technology, Harbin Institute of TechnologySchool of Life Science and Technology, Harbin Institute of TechnologyThe Second Affiliated Hospital of Heilongjiang University of Chinese MedicineSchool of Life Science and Technology, Harbin Institute of TechnologySchool of Life Science and Technology, Harbin Institute of TechnologySchool of Life Science and Technology, Harbin Institute of TechnologySchool of Life Science and Technology, Harbin Institute of TechnologySchool of Life Science and Technology, Harbin Institute of TechnologySchool of Life Science and Technology, Harbin Institute of TechnologySchool of Life Science and Technology, Harbin Institute of TechnologyDepartment of Cardiology, The Fourth Affiliated Hospital of Harbin Medical UniversitySchool of Instrumentation Science and Engineering, Harbin Institute of TechnologySchool of Life Science and Technology, Harbin Institute of TechnologyAbstract 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.https://doi.org/10.1038/s42003-025-08139-z
spellingShingle Cao Wang
Fuxing Zhu
Lan Zhou
Situo Zhang
Ruiqi Wang
Hui Tian
Bosong Zhang
Jiahui Wu
Xiang Xu
Ruixian Jiang
Xiaolu Hou
Jian Liu
Weiming Tian
Krüppel like factor 7 regulates mitochondrial dynamics balance in myocardial infarction
Communications Biology
title Krüppel like factor 7 regulates mitochondrial dynamics balance in myocardial infarction
title_full Krüppel like factor 7 regulates mitochondrial dynamics balance in myocardial infarction
title_fullStr Krüppel like factor 7 regulates mitochondrial dynamics balance in myocardial infarction
title_full_unstemmed Krüppel like factor 7 regulates mitochondrial dynamics balance in myocardial infarction
title_short Krüppel like factor 7 regulates mitochondrial dynamics balance in myocardial infarction
title_sort kruppel like factor 7 regulates mitochondrial dynamics balance in myocardial infarction
url https://doi.org/10.1038/s42003-025-08139-z
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