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