Wnt16 is a member of the Wnt family of secreted cysteine-rich glycoproteins. It is involved in joint development, skeletal homeostasis, and has been associated with the Wnt signaling pathway. Wnt16 is of great biological importance as it is strongly associated with bone mineral density, cortical bone thickness, bone strength, and osteoporotic fracture risk [1,2].

In KO/CKO mouse models, Wnt16 deficiency has shown various effects. In bone, it causes postnatal bone loss, reduces systolic blood pressure, and leads to abnormal vascular smooth muscle (VSM) mitochondrial morphology with reduced mitochondrial respiration [3]. In chondrocytes, Wnt16 deficiency exaggerates osteoarthritis (OA) progression [4]. In zebrafish, wnt16 is required for spine and muscle morphogenesis, affecting the morphogenesis of these tissues throughout the lifespan [5].

In conclusion, Wnt16 plays a crucial role in bone and joint-related biological processes. Studies using KO/CKO mouse models and zebrafish have revealed its significance in maintaining bone mass, regulating OA progression, and influencing muscle and spine morphogenesis. These findings highlight its potential as a therapeutic target for skeletal diseases and OA [1,4].