Mitochondria not only synthesize energy required for cellular functions but are also involved in numerous cellular pathways including apoptosis, calcium homoeostasis, inflammation and immunity. Mitochondria are dynamic organelles that undergo cycles of fission and fusion, and these transitions between fragmented and hyperfused networks ensure mitochondrial function, enabling adaptations to metabolic changes or cellular stress. Defects in mitochondrial morphology have been associated with numerous diseases, highlighting the importance of elucidating the molecular mechanisms regulating mitochondrial morphology. Here, we discuss recent structural insights into the assembly and mechanism of action of the core mitochondrial dynamics proteins, such as the dynamin-related protein 1 (DRP1) that controls division, and the mitofusins (MFN1 and MFN2) and optic atrophy 1 (OPA1) driving membrane fusion. Furthermore, we provide an updated view of the complex interplay between different proteins, lipids and organelles during the processes of mitochondrial membrane fusion and fission. Overall, we aim to present a valuable framework reflecting current perspectives on how mitochondrial membrane remodelling is regulated.

线粒体不仅合成细胞功能所需的能量，还参与许多细胞途径，包括细胞凋亡、钙稳态、炎症和免疫。线粒体是经历裂变和融合循环的动态细胞器，这些碎片化和过度融合网络之间的转换确保了线粒体功能，从而能够适应代谢变化或细胞应激。线粒体形态的缺陷与许多疾病有关，这凸显了阐明调节线粒体形态的分子机制的重要性。在这里，我们讨论了对核心线粒体动力学蛋白组装和作用机制的最新结构见解，例如控制分裂的动力蛋白相关蛋白 1 （DRP1） 以及驱动膜融合的线粒体融合蛋白 （MFN1 和 MFN2） 和视萎缩 1 （OPA1）。此外，我们在线粒体膜融合和裂变过程中提供了不同蛋白质、脂质和细胞器之间复杂相互作用的最新视图。总体而言，我们的目标是提出一个有价值的框架，反映当前关于如何调节线粒体膜重塑的观点。