Researchers Identify Novel Marker and Possible Therapeutic Target for Cardiovascular Calcification
Cardiovascular calcification (mineral deposits in heart valves and blood vessels) is a crucial contributor to heart disease, the leading cause of death among men and women in the United States according to the Centers for Disease Control and Prevention.
Recently, a team of researchers has discovered certain proteins in osteoclasts, a precursor to bone, that may be used in helping to destroy cardiovascular calcification by dissolving mineral deposits. The findings suggest a potential therapeutic avenue for patients with cardiovascular calcification.
“Unfortunately, there currently is no medical treatment for cardiovascular calcification, which can lead to acute cardiovascular events, such as myocardial infarction and stroke, as well as heart failure,” said Elena Aikawa, MD, PhD, director, BWH Vascular Biology Program at the Center for Interdisciplinary Cardiovascular Sciences, senior study author. “We have not found a way to reverse or slow this disease process, which is associated with aging and common chronic conditions like atherosclerosis, diabetes and kidney disease.”
Mature osteoclasts are not typically found in the vasculature. Using unbiased global proteomics (study of proteins), the researchers examined osteoclast-like cells in the vasculature to determine which proteins induced osteoclast formation. They identified more than 100 novel proteins associated with osteoclast development. Follow-up study validated top five candidate proteins, which may serve as targets for possible medications that may help promote osteoclast development in the vasculature.
“To advance this research, we need to further understand why osteoclasts are not prevalent in the vasculature, despite active calcification of the heart valves and blood vessels, and determine the difference between calcification in vasculature compared with calcification in bone,” said Aikawa. “Then we may examine ways to form functional osteoclasts in the vasculature.”
The study was published in the March 2014 issue of Arteriosclerosis, Thrombosis, and Vascular Biology.