Bmx, also known as Bone marrow kinase on chromosome X, is a cytosolic tyrosine kinase and a member of the TEC kinase family. It participates in the immune response in hematopoietic cells of the myeloid lineage, and is involved in responses to ischemia and pressure overload in the endocardium and cardiac endothelium. Bmx is also expressed in several cancers. It regulates the secretion of proinflammatory cytokines, activates the MAP kinase and NFκB pathways, and its function in IL-8 promoter regulation depends on membrane localization and kinase activity [1].

In a mouse model of arthritis, Bmx deficiency conferred protection, suggesting its role in inflammation [1]. In cecal ligation and puncture models of sepsis in mice, Bmx-KO mice showed increased thrombin-mediated endothelial permeability and vascular leakage, indicating Bmx represses these processes during early sepsis by phosphorylating PAR1 [2]. In retinal ischemia/reperfusion injury studies in Bmx-/-mice, Bmx knockdown mitigated neuroinflammation by modulating the AKT/ERK/STAT3 signaling cascade [3]. In glioma stem cells, ibrutinib, which can inhibit Bmx, disrupted the Bmx-STAT3 axis, impairing malignant growth and radioresistance [4].

In conclusion, Bmx plays essential roles in inflammation, cardiovascular responses, and cancer. Gene knockout mouse models have been crucial in revealing its functions in these areas. Understanding Bmx can provide insights into the mechanisms of related diseases and potentially lead to new therapeutic strategies.