Mitochondria are dynamic organelles that undergo cycles of fission and fusion to maintain their shape, distribution, and size. These dynamic transitions are crucial for various cellular processes such as cell cycle, immunity, apoptosis, and mitochondrial quality control. Mutations in core machinery components and defects in mitochondrial dynamics are associated with numerous human diseases. The main proteins involved in these processes are large GTPases belonging to the Dynamin family. Mitochondrial fission involves the division of one mitochondrion into two daughter mitochondria, regulated by the recruitment of Dynamin-related protein 1 (Drp1) and Dynamin 2 (Dnm2). Mitochondrial fusion is driven by mitofusins 1 and 2 (Mfn1 and Mfn2) and optic atrophy 1 (OPA1), which mediate outer and inner membrane fusion, respectively. Post-translational modifications of these proteins, such as phosphorylation, SUMOylation, and ubiquitination, play a significant role in regulating their function. Understanding the molecular mechanisms controlling mitochondrial dynamics is essential for elucidating how mitochondrial shape meets function and for advancing our knowledge of diseases associated with morphology defects. This article provides an overview of the molecular mechanisms governing mitochondrial fission and fusion in mammals.Mitochondria are dynamic organelles that undergo cycles of fission and fusion to maintain their shape, distribution, and size. These dynamic transitions are crucial for various cellular processes such as cell cycle, immunity, apoptosis, and mitochondrial quality control. Mutations in core machinery components and defects in mitochondrial dynamics are associated with numerous human diseases. The main proteins involved in these processes are large GTPases belonging to the Dynamin family. Mitochondrial fission involves the division of one mitochondrion into two daughter mitochondria, regulated by the recruitment of Dynamin-related protein 1 (Drp1) and Dynamin 2 (Dnm2). Mitochondrial fusion is driven by mitofusins 1 and 2 (Mfn1 and Mfn2) and optic atrophy 1 (OPA1), which mediate outer and inner membrane fusion, respectively. Post-translational modifications of these proteins, such as phosphorylation, SUMOylation, and ubiquitination, play a significant role in regulating their function. Understanding the molecular mechanisms controlling mitochondrial dynamics is essential for elucidating how mitochondrial shape meets function and for advancing our knowledge of diseases associated with morphology defects. This article provides an overview of the molecular mechanisms governing mitochondrial fission and fusion in mammals.