Rab32, a member of the Rab small GTPase family, is a key regulator in multiple cellular processes. It is involved in membrane trafficking pathways, especially in endosomal trafficking, and plays roles in the biogenesis of lysosome-related organelles [5]. Rab32 also participates in host defense pathways against intracellular bacterial pathogens, and is associated with regulating mitochondrial dynamics and autophagosomal components recycling [2,4].

In glioblastoma multiforme (GBM), Rab32 expression is significantly elevated, especially in the mesenchymal subtype. Knockdown of Rab32 attenuates GBM migration and invasion, suppressing invasion-related proteins and mesenchymal transition markers. Rab32 regulates ERK1/2/Drp1-dependent mitochondrial fission, promoting GBM aggressiveness [1]. In Parkinson's disease, the RAB32 variant c.213C>G (Ser71Arg) is a genetic risk factor. Functional studies show that RAB32 Arg71 activates LRRK2 kinase more than RAB32 Ser71 [3]. In rats with peripheral nerve injury, silencing Rab32 attenuates Schwann cell pyroptosis and promotes peripheral nerve regeneration, as Rab32 exacerbates pyroptosis by elevating ROS levels [6].

In summary, Rab32 is crucial in membrane trafficking, host defense, and cellular stress-related processes. Model-based research, especially knockdown experiments in relevant disease models, reveals its significant roles in glioblastoma, Parkinson's disease, and peripheral nerve injury, providing potential therapeutic targets for these diseases.