Aortic Vascular Calcification: Cholesterol Lowering Does Not Reduce Progression in Patients With Familial Hypercholesterolemia—or Does It? Nalini M. Rajamannan, MD, Stanley Nattel, MD Canadian Journal of Cardiology Volume 33, Issue 5, Pages 594-596 (May 2017) DOI: 10.1016/j.cjca.2017.03.001 Copyright © 2017 Canadian Cardiovascular Society Terms and Conditions
Figure 1 (A) Aorta in patients with normal cholesterol. (B) Calcified aorta and aortic valve in patients with heterozygous familial hypercholesterolemia. (C) Potential cellular mechanisms of Lrp5/Wnt-mediated bone formation in the valve and the aorta. Low-density lipoprotein cholesterol, a known stimulator of atherosclerosis and inflammation, signals Lrp5 to initiate Wnt signaling in the vasculature and valve interstitial cells. These cells then develop activated bone formation signaling, causing ectopic bone matrix synthesis and calcification over time. Cbfal, core-binding factor alpha 1; DKK1, Dickkopf-related protein 1; Lef, lymphoid-enhancing binding factor 1; LRP5, low-density lipoprotein receptor 5; TCF, T cell factor. Canadian Journal of Cardiology 2017 33, 594-596DOI: (10.1016/j.cjca.2017.03.001) Copyright © 2017 Canadian Cardiovascular Society Terms and Conditions