Mitochondrial fusion protein: a new therapeutic target for lung injury diseases

Mitochondria are essential organelles responsible for cellular energy supply. The maintenance of mitochondrial structure and function relies heavily on quality control systems, including biogenesis, fission, and fusion. Mitochondrial fusion refers to the interconnection of two similar mitochondria,...

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Main Authors: Guiyang Jia, Erqin Song, Qianxia Huang, Miao Chen, Guoyue Liu
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-03-01
Series:Frontiers in Physiology
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Online Access:https://www.frontiersin.org/articles/10.3389/fphys.2025.1500247/full
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author Guiyang Jia
Erqin Song
Qianxia Huang
Miao Chen
Guoyue Liu
author_facet Guiyang Jia
Erqin Song
Qianxia Huang
Miao Chen
Guoyue Liu
author_sort Guiyang Jia
collection DOAJ
description Mitochondria are essential organelles responsible for cellular energy supply. The maintenance of mitochondrial structure and function relies heavily on quality control systems, including biogenesis, fission, and fusion. Mitochondrial fusion refers to the interconnection of two similar mitochondria, facilitating the exchange of mitochondrial DNA, metabolic substrates, proteins, and other components. This process is crucial for rescuing damaged mitochondria and maintaining their normal function. In mammals, mitochondrial fusion involves two sequential steps: outer membrane fusion, regulated by mitofusin 1 and 2 (MFN1/2), and inner membrane fusion, mediated by optic atrophy 1 (OPA1). Dysfunction in mitochondrial fusion has been implicated in the development of various acute and chronic lung injuries. Regulating mitochondrial fusion, maintaining mitochondrial dynamics, and improving mitochondrial function are effective strategies for mitigating lung tissue and cellular damage. This study reviews the expression and regulatory mechanisms of mitochondrial fusion proteins in lung injuries of different etiologies, explores their relationship with lung injury diseases, and offers a theoretical foundation for developing novel therapeutic approaches targeting mitochondrial fusion proteins in lung injury.
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publisher Frontiers Media S.A.
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series Frontiers in Physiology
spelling doaj-art-9089fb5db35e4ca2865b06b54672b1322025-08-20T02:06:44ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2025-03-011610.3389/fphys.2025.15002471500247Mitochondrial fusion protein: a new therapeutic target for lung injury diseasesGuiyang Jia0Erqin Song1Qianxia Huang2Miao Chen3Guoyue Liu4Department of Critical Care Medicine, The Second Affiliated Hospital of Zunyi Medical University, Zunyi, ChinaDepartment of Critical Care Medicine, The Second Affiliated Hospital of Zunyi Medical University, Zunyi, ChinaDepartment of Critical Care Medicine, Affiliated Hospital of Zunyi Medical University, Zunyi, ChinaDepartment of Critical Care Medicine, Affiliated Hospital of Zunyi Medical University, Zunyi, ChinaDepartment of Critical Care Medicine, The Second Affiliated Hospital of Zunyi Medical University, Zunyi, ChinaMitochondria are essential organelles responsible for cellular energy supply. The maintenance of mitochondrial structure and function relies heavily on quality control systems, including biogenesis, fission, and fusion. Mitochondrial fusion refers to the interconnection of two similar mitochondria, facilitating the exchange of mitochondrial DNA, metabolic substrates, proteins, and other components. This process is crucial for rescuing damaged mitochondria and maintaining their normal function. In mammals, mitochondrial fusion involves two sequential steps: outer membrane fusion, regulated by mitofusin 1 and 2 (MFN1/2), and inner membrane fusion, mediated by optic atrophy 1 (OPA1). Dysfunction in mitochondrial fusion has been implicated in the development of various acute and chronic lung injuries. Regulating mitochondrial fusion, maintaining mitochondrial dynamics, and improving mitochondrial function are effective strategies for mitigating lung tissue and cellular damage. This study reviews the expression and regulatory mechanisms of mitochondrial fusion proteins in lung injuries of different etiologies, explores their relationship with lung injury diseases, and offers a theoretical foundation for developing novel therapeutic approaches targeting mitochondrial fusion proteins in lung injury.https://www.frontiersin.org/articles/10.3389/fphys.2025.1500247/fullmitochondrialung injurymitochondrial fusionmitofusin 1/2optic atrophy 1
spellingShingle Guiyang Jia
Erqin Song
Qianxia Huang
Miao Chen
Guoyue Liu
Mitochondrial fusion protein: a new therapeutic target for lung injury diseases
Frontiers in Physiology
mitochondria
lung injury
mitochondrial fusion
mitofusin 1/2
optic atrophy 1
title Mitochondrial fusion protein: a new therapeutic target for lung injury diseases
title_full Mitochondrial fusion protein: a new therapeutic target for lung injury diseases
title_fullStr Mitochondrial fusion protein: a new therapeutic target for lung injury diseases
title_full_unstemmed Mitochondrial fusion protein: a new therapeutic target for lung injury diseases
title_short Mitochondrial fusion protein: a new therapeutic target for lung injury diseases
title_sort mitochondrial fusion protein a new therapeutic target for lung injury diseases
topic mitochondria
lung injury
mitochondrial fusion
mitofusin 1/2
optic atrophy 1
url https://www.frontiersin.org/articles/10.3389/fphys.2025.1500247/full
work_keys_str_mv AT guiyangjia mitochondrialfusionproteinanewtherapeutictargetforlunginjurydiseases
AT erqinsong mitochondrialfusionproteinanewtherapeutictargetforlunginjurydiseases
AT qianxiahuang mitochondrialfusionproteinanewtherapeutictargetforlunginjurydiseases
AT miaochen mitochondrialfusionproteinanewtherapeutictargetforlunginjurydiseases
AT guoyueliu mitochondrialfusionproteinanewtherapeutictargetforlunginjurydiseases