The role of sclerostin in the development and progression of cardiovascular diseases- a potential biomarker?

Sclerostin, a glycoprotein primarily synthesized by osteocytes, is a key regulator of bone remodeling through its inhibition of the Wnt/β-catenin signaling pathway. Beyond its established role in bone metabolism, sclerostin has been identified in vascular tissues, including smooth muscle cells of blood vessels, suggesting a potential role in cardiovascular diseases (CVD). Research on sclerostin's role in CVD has yielded conflicting results, highlighting its complex involvement in vascular calcification and atherosclerosis. Some studies associate elevated sclerostin levels with a reduced risk of cardiovascular events, potentially due to its inhibition of pathways driving vascular calcification and osteogenic transformation of vascular cells. Conversely, other research links higher sclerostin levels with increased cardiovascular risk, including atherosclerosis, myocardial infarction, and stroke, possibly reflecting a compensatory response to vascular damage or inflammation. Discrepancies in findings may stem from differences in study populations, methodologies, and confounding factors such as age, renal function, and medication use. Furthermore, sclerostin's dual effects may depend on specific pathological contexts, complicating its interpretation as a biomarker. This review examines the evidence for sclerostin's role in CVD and its potential utility as a biomarker for cardiovascular risk stratification. While emerging data suggest diagnostic and therapeutic relevance, particularly in populations with chronic kidney disease or metabolic disorders, further research is necessary to elucidate its mechanisms, identify modulating factors, and assess its clinical value. A clearer understanding of sclerostin's vascular effects could pave the way for novel approaches to cardiovascular disease prevention and management.