Bifunctional growth regulator that stimulates the growth of cultured chondrocytes in the presence of basic fibroblast growth factor (FGF) but inhibits the growth of cultured vascular endothelial cells. May contribute to the rapid growth of cartilage and vascular invasion prior to the replacement of cartilage by bone during endochondral bone development (By similarity). Inhibits in vitro tube formation and mobilization of endothelial cells (By similarity). Plays a role as antiangiogenic factor in cardiac valves to suppress neovascularization. Accumulated in the inter-territorial matrix of cartilage. Detected in the four cardiac valves, valvular interstitial cells and extracellular matrix (at protein level). Detected from 9.5 dpc in the cardiac valve precursor cells from the atrioventricular cushions and outflow. At 10 dpc expressed in the cardiac jelly covering the trabeculating cardiomyocytes of the left ventricle, the outer curvature of the right ventricle and the outflow tract. Expression in the ventricles decreased gradually as development progressed, and disappeared by mid-embryogenesis (at protein level). After cleavage, the post-translationally modified ChM-I is secreted as a glycoprotein. Aged mice show enhanced VEGFA expression, angiogenesis, inflammatory cell infiltration, aortic stenosis, lipid deposition and calcification in the cardiac valves. Belongs to the chondromodulin-1 family.