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Editorial
. 2015 Aug 25;132(8):621-3.
doi: 10.1161/CIRCULATIONAHA.115.018139. Epub 2015 Jul 29.

A Not-So-Little Role for Lipoprotein(a) in the Development of Calcific Aortic Valve Disease

Maximillian A Rogers  1 , Elena Aikawa  2
Affiliations
Editorial

A Not-So-Little Role for Lipoprotein(a) in the Development of Calcific Aortic Valve Disease

Maximillian A Rogers et al. Circulation. .
No abstract available

Keywords: Editorials; PCSK9 protein, human; heart valves; vascular calcification.

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Figures

Figure 1
Figure 1
Potential role of Lp(a) and PCSK9 in CAVD. Lp(a) may get taken up and metabolized by cells via Lp(a) receptors (receptors for which Lp(a) is a ligand). However, in the presence of PCSK9 some of these receptors may be internalized and degraded instead of recycled back to the cell surface (A). As such more Lp(a) derived oxidized lipids may be converted to LPA and be taken up by VICs via LPA receptors. This may lead to the production of inflammation related cytokines (e.g., IL6) through NF-κB nuclear localization that in turn increase BMP and/or other calcification inducing processes leading to valve calcification. PCSK9 inhibitors may act to block PCSK9 interaction with Lp(a) receptors, resulting in Lp(a) receptors being recycled back to the cell surface where they can take up more Lp(a) (B). Dashed arrows indicate multiple steps in the pathway.
See this image and copyright information in PMC

Comment on

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