Cnmd-flox Mouse

Chondromodulin-I (Cnmd), also known as Chm-1, Chm-I, or Lect1, is a gene encoding a 334-amino-acid type II transmembrane glycoprotein. It is primarily expressed in cartilage and plays crucial roles in chondrocyte proliferation, cartilage homeostasis, and angiogenesis blocking. It is also involved in bone repair and may delay osteoarthritis (OA) progression. Its down-regulation is correlated with OA severity, suggesting its potential as a therapeutic target [1,3].

In a mouse model of distraction osteogenesis, Cnmd null (Cnmd-/-) mice showed less cartilage callus formation, with the distraction gap filled by fibrous tissues. Radiological and histological investigations demonstrated delayed bone consolidation and remodeling of the lengthened segment. Cnmd deficiency also caused a one-week delay in the peak expression of VEGF, MMP2, and MMP9 genes and subsequent angiogenesis and osteoclastogenesis, indicating that Cnmd is necessary for cartilage callus distraction [2].

In conclusion, Cnmd is essential for cartilage-related biological processes such as chondrocyte growth, cartilage callus distraction, and bone repair. Mouse models with Cnmd deficiency have revealed its importance in these processes, and its potential role in OA. Understanding Cnmd may provide new therapeutic strategies for OA and other cartilage-related diseases [1,2,3].