Pathobiology of Lp(a) in calcific aortic valve disease. (3rd October 2017)

• Record Type: Journal Article
• Authors: Mathieu, Patrick; Arsenault, Benoit J.; Boulanger, Marie-Chloé; Bossé, Yohan; Koschinsky, Marlys L.
• Is Part Of: Expert review of cardiovascular therapy. Volume 15:Number 10(2017)
• Page Start: 797
• Page End: 807
• Publication Date: 2017-10-03
• Subjects: Calcific aortic valve disease -- calcific aortic stenosis -- Lp(a) -- apolipoprotein(a) -- autotaxin; Cardiovascular agents -- Research -- Periodicals; 616.12061
• DOI: 10.1080/14779072.2017.1367286
• Languages: English
• ISSNs: 1477-9072

Abstract

ABSTRACT: Introduction : Calcific aortic valve disease (CAVD) is the most prevalent heart valve disorder. Gene variant in the LPA gene, which encodes for apolipoprotein(a), has been associated at the genome-wide level with CAVD. The process whereby Lp(a) promotes the development of CAVD is under intensive investigation and recent data have shed important insights into disease biology. In this regard, autotaxin (ATX), a lysophospholipase D, interacts with Lp(a) and promotes the mineralization of the aortic valve. Areas covered : In this paper, we are reviewing the biology of Lp(a) and the latest discoveries about the molecular processes that link this lipoprotein with the development of CAVD including the role of ATX. Expert commentary : Elevated Lp(a) levels are genetically determined and considered as an important risk factor for CAVD. Understanding how Lp(a) promotes the development/progression of CAVD is crucial as it may hold promise for the development of new therapies.