遗传 ›› 2026, Vol. 48 ›› Issue (8): 764-780.doi: 10.16288/j.yczz.25-343

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机械力敏感离子通道在胚胎发育中调控线粒体功能的研究进展

张渭莹1(), 宁欣2, 罗博煜3, 魏凯1, 滕越3(), 商微1()   

  1. 1 中国人民解放军总医院妇产医学部北京 100700
    2 河北省沧州中西医结合医院沧州 061000
    3 军事科学院军事医学研究院北京 100071
  • 收稿日期:2025-12-25 修回日期:2026-03-02 出版日期:2026-08-20 发布日期:2026-04-29
  • 通讯作者: 商微,硕士,主任医师,研究方向:生殖医学、线粒体遗传病。E-mail: shang.wei@163.com;
    滕越,博士,研究员,研究方向:合成生物学。E-mail: yueteng@me.com
  • 作者简介:张渭莹,博士,助理研究员,研究方向:发育生物学。E-mail: zhangwyjessie@163.com
  • 基金资助:
    中国康复医学会2024年科研课题重点项目计划(KFKT-2024-KY-019)

Mechanosensitive ion channels in embryonic development: advances in the regulation of mitochondrial function

Weiying Zhang1(), Xin Ning2, Boyu Luo3, Kai Wei1, Yue Teng3(), Wei Shang1()   

  1. 1 Senior Department of Obstetrics & Gynecology, PLA General Hospital, Beijing 100700, China
    2 Cangzhou Hospital of Integrated Traditional Chinese and Western Medicine, Hebei Province, Cangzhou 061000, China
    3 State Key Laboratory of Pathogen and Biosecurity, Academy of Military Medical Sciences, Beijing 100071, China
  • Received:2025-12-25 Revised:2026-03-02 Published:2026-08-20 Online:2026-04-29
  • Supported by:
    Key Research Project of the Chinese Association of Rehabilitation Medicine(KFKT-2024-KY-019)

摘要:

机械力是胚胎发育与生殖过程中持续存在且高度动态的物理输入,可通过机械力敏感离子通道(mechanosensitive ion channels, MSC)被细胞感知,并转化为以Ca2+为核心的胞内信号,从而参与调控细胞迁移、谱系分化与形态发生等关键发育事件。与此同时,线粒体作为能量代谢与信号整合枢纽,其代谢模式、氧化还原稳态及动力学重塑对胚胎早期发育潜能具有重要影响。近年来的研究提示,MSC介导的Ca2+通量变化不仅激活经典信号通路,还可进一步耦联线粒体功能,形成连接力学输入与代谢响应的重要调控轴。基于上述研究背景,本文围绕“MSC-线粒体功能-胚胎发育命运”这一主线,系统梳理MSC的分子特征与激活机制,概述其在胚胎发育及生殖相关过程中的功能;进一步归纳MSC通过Ca2+信号调控线粒体代谢重编程、ROS稳态及融合/分裂动态的潜在机制;并结合囊胚腔形成与谱系建立、器官发生等典型发育事件,讨论该耦联轴在关键发育过程中的可能作用。同时,对当前研究面临的关键局限与技术瓶颈进行分析,并提出该领域未来的研究方向与潜在应用前景。在发育生物学背景下整合机械转导与线粒体代谢调控机制,有助于深化对“力学-代谢”信号协同塑造胚胎命运与形态建成过程的理解,并为相关发育异常与生殖障碍的发病机制解析及干预策略探索提供理论依据。

关键词: 机械力敏感离子通道, 线粒体, 胚胎发育, 生殖, 机械转导

Abstract:

Mechanical forces are persistent and dynamic physical cues during embryonic development and reproduction. Through mechanosensitive ion channels (MSCs), these forces are converted into intracellular signals-primarily mediated by Ca2+ flux, that regulate cell migration, lineage specification, and morphogenesis. In parallel, mitochondria serve as central hubs of energy metabolism and signal integration, and their metabolic state, redox homeostasis, and dynamic remodeling critically influence early developmental competence. Increasing evidence suggests that MSC-mediated Ca2+ signaling not only activates canonical signaling pathways but also functionally couples to mitochondrial activity, establishing a regulatory axis that links mechanical inputs to metabolic responses. This review focuses on the “MSC-mitochondrial function- embryonic developmental fate” axis. We systematically summarize the molecular characteristics and activation mechanisms of MSCs and discuss their roles in embryonic development and reproductive processes. Furtherly, we examine how MSC-dependent Ca2+ signaling modulates mitochondrial metabolic reprogramming, reactive oxygen species (ROS) homeostasis, and fusion-fission dynamics, and consider the potential implications of this coupling in key developmental events including blastocoel formation, lineage specification, and organogenesis. We also discuss the current limitations and technical challenges in the field, together with future research directions and potential translational implications. By integrating mechanotransduction with mitochondrial metabolic regulation in the developmental context, this framework provides insights into how mechanical and metabolic signals coordinately shape embryonic cell fate and morphogenesis, and offers a theoretical basis for elucidating the mechanisms underlying developmental abnormalities and reproductive disorders, as well as exploring potential intervention strategies.

Key words: mechanosensitive ion channels, mitochondria, embryonic development, reproduction, mechanotransduction