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. 2017 Dec 1;7:16710. doi: 10.1038/s41598-017-17165-9

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© The Author(s) 2017

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Schematic diagram illustrating the potential role of lnc-KDM5D-4 in atherosclerosis. Atherosclerosis is driven by a chronic inflammatory process. Lipid disturbances and other risk factors are thought to cause endothelial injury resulting in monocyte adhesion and migration to the intima, as well as the release of cytokines and growth factors. Low-density lipoprotein (LDL) particles travelling in the blood and carrying cholesterol and triglycerides from the liver to other body tissues get through the endothelium layer due to their size and density, and become oxidized. After migration to the sub-endothelial space, monocytes differentiate into macrophages, which are then able to ingest oxidized-LDL, forming specialized foam cells. Macrophages are not able to process the oxidized-LDL and ultimately grow and rupture depositing a greater amount of oxidized cholesterol into the artery wall. This triggers the recruitment of more monocytes, thus increasing the inflammation and continuing the cycle. This inflammation leads to subendothelial accumulation of fatty substances called atheromatous plaques. In the hepatocytes, the underexpression of the Y chromosome-linked lincRNA lnc-KDM5D-4 results in an overexpression of the gene perilipin 2 (PLIN2) involved in lipid droplet formation within the cells. This increase of expression of PLIN2 may consequently initiates the ‘fatty liver’ or hepatic steatosis promoting atherosclerosis in the coronary arteries of men.