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Vascular Calcification

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Front. Cardiovasc. Med. | doi: 10.3389/fcvm.2018.00172

Lipoproteins in cardiovascular calcification: Potential targets and challenges

  • 1UCLA Department of Medicine, United States
  • 2University of California, Los Angeles, United States

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, 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.

Keywords: Lipoproteins, calcification, Lp(a), autotaxin, Osteogenesis

Received: 23 Aug 2018; Accepted: 08 Nov 2018.

Edited by:

Dwight A. Towler, University of Texas Southwestern Medical Center, United States

Reviewed by:

Alexander N. Kapustin, AstraZeneca (United Kingdom), United Kingdom
Sasha A. Singh, Brigham and Women's Hospital, Harvard Medical School, United States  

Copyright: © 2018 Tintut, Hsu and Demer. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Linda L. Demer, UCLA Department of Medicine, Los Angeles, 90404, California, United States, ldemer@mednet.ucla.edu