Abstract
Previously considered a degenerative process, cardiovascular calcification is now established as an active process that is regulated in several ways by lipids, phospholipids, and lipoproteins. These compounds serve many of the same functions in vascular and valvular calcification as they do in skeletal bone calcification. Hyperlipidemia leads to accumulation of lipoproteins in the subendothelial space of cardiovascular tissues, which leads to formation of mildly oxidized phospholipids, which are known bioactive factors in vascular cell calcification. One lipoprotein of particular interest is Lp(a), which showed genome-wide significance for the presence of aortic valve calcification and stenosis. It carries an important enzyme, autotaxin, which produces lysophosphatidic acid (LPA), and thus has a key role in inflammation among other functions. Matrix vesicles, extruded from the plasma membrane of cells, are the sites of initiation of mineral formation. Phosphatidylserine, a phospholipid in the membranes of matrix vesicles, is believed to complex with calcium and phosphate ions, creating a nidus for hydroxyapatite crystal formation in cardiovascular as well as in skeletal bone mineralization. This review focuses on the contributions of lipids, phospholipids, lipoproteins, and autotaxin in cardiovascular calcification, and discusses possible therapeutic targets.
Highlights
Considered a degenerative process, cardiovascular calcification is established as an active process that is regulated in several ways by lipids, phospholipids, and lipoproteins
These compounds serve many of the same functions in vascular and valvular calcification as they do in skeletal bone calcification
Hyperlipidemia leads to accumulation of lipoproteins in the subendothelial space of cardiovascular tissues, which leads to formation of mildly oxidized phospholipids, which are known bioactive factors in vascular cell calcification
Summary
Considered a degenerative process, cardiovascular calcification is established as a regulated process [1,2,3] in which vascular and valvular mesenchymal cells undergo osteogenic differentiation [4,5,6,7,8]. Vascular calcification is considered pathognomonic of atherosclerosis. The degree of calcification has been shown to correlate closely with the degree of atherosclerotic plaque burden [9]. The presence of calcium deposits in atherosclerotic lesions appears to increase the risk of intraplaque hemorrhage [10], in which mechanical disruption within a lesion tears microvessels, causing bleeding. The bleeding expands the lesion, so that it may abruptly encroach on the artery lumen causing stenosis or occlusion, which result in ischemia or infarction
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