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. 2021 Feb 16;11:3881. doi: 10.1038/s41598-021-82966-y

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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The proteins/enzymes in this pathway regulate both calcification and atherosclerosis. ABCC6 activity facilitates the cellular efflux of ATP from liver and other tissues/cells, which is quickly converted to pyrophosphate (PPi), a potent inhibitor of mineralization. Decreased plasma PPi levels cause calcification in PXE (OMIM #264800) and GACI (OMIM #614473 and #208000). NT5E activity leads to adenosine production which has numerous biological activities towards inflammation, atherosclerosis and inhibition of TNAP synthesis. TNAP degrades PPi into inorganic phosphate (Pi), an activator of calcification which leads to vascular calcification in Calcification of Joints and Arteries patients (CALJA, OMIM #211800). In addition to ABCC6, both ENPP1 and NT5E functions have been linked to atherosclerosis development in ApoE^−/− mice. ENTPD1 function overlaps with that of ENPP1 and also plays a role in atherosclerosis in mice lacking ApoE, though this ectoenzyme does not seem to regulate ectopic calcification. Symbols: ∅ : no known effect; ➚: increase; ➘: decrease.