Wnt7 refers mainly to WNT7A and WNT7B, secreted Wnt ligands that regulate embryonic development, CNS angiogenesis, and blood-brain barrier formation
[1][2]. Mechanistically, WNT7A/B activate endothelial β-catenin signaling through GPR124-RECK-LRP5/6 receptor complexes, with WNT7 signaling showing isoform-selective dependence on RECK compared with WNT3A
[2][3]. In disease models, WNT7B drives autocrine Wnt/β-catenin signaling and anchorage-independent growth in pancreatic adenocarcinoma cells, while Wnt7a/7b deletion or pharmacologic Wnt inhibition blocks glioma vessel co-option and improves temozolomide response
[4][5]. Compared with related Wnt isoforms, WNT7A and WNT7B directly bind RECK, whereas WNT3A does not, supporting Wnt7-specific regulation of ligand bioavailability and endothelial signaling
[3]. For experimental applications, Wnt secretion inhibitors such as IWP-2 suppress ligand-dependent Wnt/β-catenin activity in PDAC cells, while FZD4-LRP5 agonists can induce a Norrin-like barrier transcriptional response in retinal models
[4][6].