Mitochondrial Dynamics and Remodelling

Dear Colleagues,

Mitochondrial dynamics govern the balance between fission, fusion, motility, and selective turnover, shaping cell fate. These processes rely on dynamin-related GTPases, cristae-structuring complexes, and quality-control mechanisms including mitophagy and mitochondrial-derived vesicles. Their coordination is further integrated with ER–mitochondria contact sites, cytoskeletal transport, and signaling pathways that adjust mitochondrial morphology to cellular needs. Key questions remain unresolved: how distinct cell types (neurons, cardiomyocytes, immune cells) establish specific fission–fusion set points, how lipids and post-translational modifications regulate rapid remodeling under stress, and how cristae changes intersect with bioenergetics in neurodegeneration, cancer, and metabolic disorders. Moreover, it is unclear which roles of quality control are causal versus compensatory in disease. Advances in live-cell imaging, cryo-electron tomography, spatial omics, and genetically encoded reporters have provided new insights, but spatiotemporal integration of these processes is still required. This Special Issue aims to synthesize current understanding of mitochondrial structural machines (DRP1, MFF, FIS1, OPA1, MFN1/2, MICOS), signaling hubs (AMPK, mTORC1/2, Ca²⁺/calcineurin), and their links to bioenergetics, immune function, and disease. We highlight therapeutic opportunities through small-molecule modulators, gene-based interventions, and strategies to restore mitochondrial remodeling in health and pathology.

Dr. Edmund Carvalho
Guest Editor

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