Tspo, also formerly known as the peripheral benzodiazepine receptor, is an 18 kDa translocator protein located in the outer mitochondrial membrane [2,4,5,8]. It is phylogenetically widespread and is implicated in regulating many cellular processes, such as inflammatory responses, oxidative stress, and mitochondrial homeostasis [2,4]. Its ligands are used as diagnostic biomarkers, especially in glioma and for imaging neuroinflammation [1,3,5,6,7].

In glioma research, Tspo knockout xenograft and spontaneous mouse glioma models were used. Tspo deficiency promoted glioma cell proliferation in vitro and glioma growth and angiogenesis in vivo. It also led to mitochondrial dysfunction, with more fragmented mitochondria, increased glucose uptake, lactic acid conversion, decreased oxidative phosphorylation, and increased glycolysis. This shows Tspo serves as a key regulator of glioma growth and malignancy by controlling the metabolic balance between mitochondrial oxidative phosphorylation and glycolysis [1].

In conclusion, Tspo is an evolutionarily conserved protein with diverse functions related to stress-induced metabolic changes and mitochondrial homeostasis. The use of Tspo knockout mouse models in glioma research has revealed its crucial role in glioma growth, angiogenesis, and metabolic regulation, highlighting its potential as a therapeutic target for glioblastoma [1,4].