B3GALT2 is a beta-1,3-galactosyltransferase that catalyzes the transfer of galactose from UDP-galactose to substrates with terminal beta-N-acetylglucosamine residues, playing a critical role in glycoprotein and glycolipid biosynthesis. The enzyme localizes to the Golgi membrane and participates in oligosaccharide biosynthetic pathways. Mechanistically, B3GALT2 exerts neuroprotective effects primarily through glycosylation modification of membrane receptors and activation of TGF-β signaling. In ischemic stroke models, B3GALT2 maintains blood-brain barrier (BBB) integrity via TGF-β1/TGF-βR(II)/p-Smad2/3 signaling 1, and promotes cerebral angiogenesis during the repair phase through glycosylation of TGF-βR(II) and ALK1 receptors 2. Additionally, B3GALT2 suppresses NLRP3 inflammasome-mediated pyroptosis and oxidative stress via TGF-β1-dependent pathways 3. Clinically, B3GALT2 deficiency exacerbates ischemic brain injury, with heterozygous knockout mice showing increased infarct volume and neuronal apoptosis; these effects are reversible by Reelin pathway modulation 4. In gouty arthritis, B3GALT2 is downregulated and inversely correlates with inflammatory markers; TFAP2A transcriptionally activates B3GALT2 to suppress pyroptosis 5. B3GALT2 also appears as a predicted target gene in stem cell exosome-mediated cartilage maintenance 6 and may regulate calcium signaling in epileptogenesis 7.