Vasn, which encodes vasorin, is a protein-coding gene involved in multiple biological processes. Vasorin is a transmembrane protein and is associated with several pathways, such as the YAP/TAZ, NOTCH, and MAPK pathways. It plays a crucial role in tumor development, angiogenesis, bone turnover, and vascular function [1-7, 9]. Genetic models, like knockout mice, are valuable for studying its functions.

In gene knockout studies, Vasn-deficient constitutive KO mice, but not osteoclast-targeted KO mice, showed an osteopenic bone phenotype due to enhanced osteoclast activity, indicating Vasn's role in bone turnover [7]. In myocardial fibrosis research, VASN-/-mice presented typical features of MF, with reduced extracellular matrix genes and up-regulated inflammatory factors, suggesting VASN knockout induces MF by regulating non-collagen fibers and inflammation [9]. In cancer research, knockdown of VASN in various cancer cell lines (prostate, colorectal, laryngeal, thyroid, and ARID1A-deficient lung adenocarcinoma) inhibited cell proliferation, migration, invasion, and in some cases, reversed epithelial-mesenchymal transition (EMT). This was often associated with the down-regulation of related signaling pathways, such as YAP/TAZ and NOTCH/MAPK [1,2,3,4,5,6]. In severe preeclampsia, decreased extracellular vesicle VASN was found to mediate endothelial dysfunction [8].

In conclusion, Vasn has diverse essential biological functions. Through gene knockout models, its roles in bone-related pathologies, myocardial fibrosis, cancer progression, and preeclampsia-related endothelial dysfunction have been revealed. These findings contribute to a better understanding of the underlying mechanisms of these diseases and may provide potential biomarker and therapeutic target candidates.