Emcn, also known as endomucin, is an endothelial-specific glycocalyx component highly expressed in certain vascular endothelium. It is involved in angiogenesis-related biological processes and is crucial for maintaining normal physiological functions. It has been implicated in pathways such as those regulating the coupling of angiogenesis and osteogenesis, and it may also be associated with the regulation of VEGF activity [3].

In bone-related studies, gene knockout models have been revealing. Mice with osteoblast-specific deletion of Shn3, which have elevated bone formation, show an increase in CD31hiEMCNhi endothelium. Genetic deletion of Slit3, an osteoblast-derived factor, reduces skeletal CD31hiEMCNhi endothelium, leading to low bone mass due to impaired bone formation [1].

In a mouse model of endothelial cell-specific knockout of EMCN (EMCNecko), endothelial EMCN deficiency does not significantly affect primary tumor growth but strongly promotes spontaneous lung metastasis by affecting the host microenvironment and forming a lung pre-metastatic niche [2].

In global EMCN knockout mice, there is glomerular impairment, with increased infiltration of immune cells, albuminuria, and abnormal glomerular structure, suggesting its role in maintaining glomerular filtration barrier function [3].

In conclusion, Emcn plays essential roles in angiogenesis-osteogenesis coupling, tumor metastasis regulation, and glomerular function. Gene knockout mouse models, such as the EMCNecko and global EMCN knockout mice, have been instrumental in understanding Emcn's functions in bone-related diseases, tumor metastasis, and kidney-related pathologies, providing insights into potential therapeutic targets for these conditions.