Sostdc1, also known as sclerostin domain-containing protein-1, encodes a secreted 28-32 kDa protein with a cystine knot-like domain and two N-linked glycosylation sites. It functions as an antagonist to bone morphogenetic protein (BMP), mediating BMP signaling, and also interacts with LRP6 to regulate Wnt signaling, thus playing roles in cellular proliferation, differentiation, and programmed cell death. Sostdc1 is important in multiple tissues including skin, intestines, brain, lungs, kidneys, vasculature, and the skeletal system [1].

In gene-knockout mouse models, deletion of Sostdc1 led to supernumerary teeth and improved renal function loss in Alport syndrome [1]. In the skeletal system, Sostdc1 deficiency alone had no measurable effects on bone envelopes, but when Sostdc1 and Sost were co-deleted in male mice, it led to high bone mass and increased cortical properties. Also, combined administration of sclerostin antibody and Sostdc1 antibody in wild-type female mice potentiated cortical bone gain [3]. In NK cell development, Sostdc1-knockout mice showed a partial developmental block with a progressive accumulation of transitional NK cells and changes in the Ly49 repertoire, and the NK cells were hyporesponsive against MHC class I-deficient cell targets [2].

In conclusion, Sostdc1 is crucial for various biological processes. Model-based research, especially the use of KO mouse models, has revealed its significant roles in skeletal biology, renal function, and NK cell maturation. These findings provide a theoretical basis for understanding related biological processes and treating associated diseases.