Coronary artery disease (CAD) is a cardiovascular disease mainly caused by atherosclerosis, which involves a variety of pathophysiological mechanisms such as lipid metabolism, inflammatory response, and endothelial dysfunction. Fetuin B is a glycoprotein secreted by the liver, which can participate in many processes such as cell inflammation, vascular calcification, and lipid metabolism, and is closely related to the pathogenesis of CAD. This article reviews the relationship between fetuin B and CAD and the mechanism of its occurrence and development, in order to provide new choices and methods for the prevention, diagnosis, and treatment of CAD.
Sclerostin, as a bone-derived secreted glycoprotein, is a suppressor of Wnt signaling pathway. Recently, adverse cardiovascular events in the treatment of osteoporosis with sclerostin inhibitors have raised concerns about the association of sclerostin with atherosclerotic heart disease. Whether the role of sclerostin in atherosclerotic heart disease is harmful or beneficial is not clear. This article reviews the progress of the mechanisms of sclerostin in vascular calcification and atherosclerotic heart disease, focusing on the relationship between sclerostin and vascular calcification, the impact of its concentration changes on atherosclerotic heart disease, and the effect of sclerostin inhibitor on cardiovascular events.