Plexin B2 in physiology and pathophysiology of the central nervous system

The Plexin protein family was initially found in 1995, comprising subfamilies from Plexin A to Plexin D. Plexin B2, a member of the Plexin subfamily, has widespread expression in many human organs and tissues, particularly in the nervous system where expression levels are significantly heightened. The biological roles of Plexin B2 are mostly determined by its protein structure and functional domains. These domains regulate the binding selectivity and affinity for ligands. Ligand binding activates signal transduction pathways, resulting in regulatory effects on several biological processes. This includes managing brain growth and change, keeping angiogenesis and vascular homeostasis in check, and preventing the start, growth, and metastasis of cancer. Plexin B2 has also been associated with the onset of many nervous system illnesses. Plexin B2 aids in the invasion and spread of malignant cells, facilitates nerve healing following spinal cord damage, and plays a role in the etiology of schizophrenia. This article thoroughly examines the existing research on Plexin B2 and its importance in central nervous system biology. Simultaneously, it investigates the regulatory function of Plexin B2 across many cell types in the central nervous system, specifically neural stem cells, neurons, microglia, and astrocytes. This study examines the current knowledge of Plexin B2's role in central nervous system diseases, including schizophrenia, spinal cord injury, neuroblastoma, and fear memory. Overall, the prospects for the clinical translation of Plexin B2 are promising. However, challenges related to specificity and drug delivery must be addressed. Future research could explore the integration of nanodrug delivery systems to enhance the clinical application of Plexin B2-targeted therapies.