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Received Jan 20, 2017; Revised Mar 3, 2017; Accepted Oct 11, 2017
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
1. Introduction
So far, three major types of blood vessel calcification have been described, including proatherosclerotic arterial calcification, Mönckeberg calcification in the intima media, and infantile calcification [1]. Calcification of atherosclerotic lesions starts in the middle age and is prevalent in the elderly population. Clinical outcomes of the atherosclerosis involve unstable or stable angina, thrombosis, heart attack, stroke, and sudden coronary death. It has been found that lethal cases from coronary thrombosis were caused by acute coronary syndrome followed by erosion and formation of calcified nodules [2]. In this paper, we will focus on the mechanisms of arterial calcification associated with atherosclerotic disease.
2. Atherosclerotic Lesion Progression
Atherosclerosis progression is a dynamic process that spans through a substantial part of the lifetime and leads to the formation of unstable lesions followed frequently by acute thrombosis, which can be lethal or life-threatening. Atherosclerosis-associated thickening of the arterial wall starts with an increase in vascular smooth muscle cells (VSMCs) count and extracellular matrix (ECM) mass in the intima and media, paralleled by infiltration of inflammatory cells as a result of the adaptive immune response. Macroscopically visible plaques begin to develop as fatty streaks located in the subendothelial region of the arterial wall, which are infiltrated with lipid-laden macrophages [3]. However, the earliest events in the lesion development are associated with the formation of cell-free lipid pools located...