Ion channel-mediated mitochondrial volume regulation and its relationship with mitochondrial dynamics

ABSTRACT

The mitochondrion, one of the important cellular organelles, has the major function of generating adenosine triphosphate and plays an important role in maintaining cellular homeostasis, governing signal transduction, regulating membrane potential, controlling programmed cell death and modulating cell proliferation. The dynamic balance of mitochondrial volume is an important factor required for maintaining the structural integrity of the organelle and exerting corresponding functions. Changes in the mitochondrial volume are closely reflected in a series of biological functions and pathological changes. The mitochondrial volume is controlled by the osmotic balance between the cytoplasm and the mitochondrial matrix. Thus, any disruption in the influx of the main ion, potassium, into the cells can disturb the osmotic balance between the cytoplasm and the matrix, leading to water movement between these compartments and subsequent alterations in mitochondrial volume. Recent studies have shown that mitochondrial volume homeostasis is closely implicated in a variety of diseases. In this review, we provide an overview of the main influencing factors and research progress in the field of mitochondrial volume homeostasis.

GRAPHICAL ABSTRACT

KEYWORDS:

• Ion channels
• mitochondrial
• cell volume regulation

Disclosure statement

No potential conflict of interest was reported by the author(s).

This manuscript has been thoroughly edited by a native English speaker from an editing company. An editing certificate will be provided upon request.

Data availability statement

Data sharing is not applicable to this article as no new data were created or analyzed in this study.

Author Contribution

Yujia Zhuang, Wenting Jiang Zhe Zhao, Jianquan Liu, Wencui Li and Zhiqin Deng participated in the literature review, Yujia Zhuang and Zhiqin Deng performed the figure design, Yujia Zhuang wrote the manuscript. The authors read and approved the final manuscript.

Additional information

Funding

This study was supported by the National Natural Science Foundation of China [81972085, 82172465], China University Industry-University-Research Innovation Fund [2021JH037], the Natural Science Foundation of Guangdong Province [2021A1515010706, 2023A1515010102], Guangdong Provincial Key Clinical Discipline-Orthopedics [2000005], the Sanming Project of Shenzhen Health and Family Planning Commission [SZSM202311008], Shenzhen Science and Technology Planning [GJHZ20210705142007023], the Shenzhen Key Medical Discipline Construction Fund [SZXK025], Scientific Research Foundation of Shenzhen Health Economics Association [2023100, 2023101, 2023106].