Mitochondria have many forms and can change their shape through fusion and fission of the outer and inner membranes, called “mitochondrial dynamics”. Mitochondrial outer membrane proteins, such as mitochondrial fission protein 1 (FIS1), mitochondrial fission factor (MFF), mitochondrial 98 dynamics proteins of 49 kDa (MiD49), and mitochondrial dynamics proteins of 51 kDa (MiD51), can aggregate at the outer mitochondrial membrane and thus attract Dynamin-related protein 1 (DRP1) from the cytoplasm to the outer mitochondrial membrane, where DRP1 can perform a scissor-like function to cut a complete mitochondrion into two separate mitochondria. Other organelles can promote mitochondrial fission alongside mitochondria. FIS1 plays an important role in mitochondrial–lysosomal contacts, differentiating itself from other mitochondrial-fission-associated proteins. The contact between the two can also induce asymmetric mitochondrial fission. The kidney is a mitochondria-rich organ, requiring large amounts of mitochondria to produce energy for blood circulation and waste elimination. Pathological increases in mitochondrial fission can lead to kidney damage that can be ameliorated by suppressing their excessive fission. This article reviews the current knowledge on the key role of mitochondrial-fission-associated proteins in the pathogenesis of kidney injury and the role of their various post-translational modifications in activation or degradation of fission-associated proteins and targeted drug therapy.

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AimsCorni Fructus (CF) and some CF‐contained prescriptions are commonly used in clinical treatment of depression. This investigation aims to evaluate the main active compound of CF in antidepressant properties and its key target.MethodsFirstly, this study established a behavioral despair model and used high‐performance liquid chromatography method to evaluate the antidepressant‐like effects of water extract, 20%, 50%, and 80% ethanol extracts of CF, and its main active compound. Then, this study created chronic unpredictable mild stress (CUMS) model to assess loganin's antidepressant‐like properties, and its target was evaluated by quantitative real‐time polymerase chain reaction, Western blot, Immunofluorescence, enzyme‐linked immunosorbent assay, and tyrosine receptor kinase B (TrkB) inhibitor.ResultsResults showed that the different extracts of CF significantly shortened the immobility time in forced swimming and tail suspension tests. Moreover, loganin alleviated CUMS‐induced depression‐like behavior, promoted neurotrophy and neurogenesis, and inhibited neuroinflammation. Furthermore, K252a blocked the improvement of loganin on depression‐like behavior, and eliminated the enhancement of neurotrophy and neurogenesis and the inhibition of neuroinflammation.ConclusionOverall, these results indicated that loganin could be used as a major active compound of CF for the antidepressant‐like properties and exerted antidepressant‐like actions by regulating brain derived neurotrophic factor (BDNF)–TrkB signaling, and TrkB could be used as key target for itsantidepressant‐like actions.