Cardiovascular Research Center, CSIC-ICCC, HSCSP, Barcelona, Spain ; CIBER OBN -Instituto Salud Carlos III, Madrid, Spain ; Cardiovascular Research Chair, UAB, Barcelona, Spain.
Eur Heart J Acute Cardiovasc Care. 2012 Apr;1(1):60-74. doi: 10.1177/2048872612441582.
Atherosclerosis is the underlying reason for nearly all causes of coronary artery disease and peripheral arterial disease and many cases of stroke. Atherosclerosis is a systemic inflammatory process characterised by the accumulation of lipids and macrophages/lymphocytes within the intima of large arteries. The deposition of these blood borne materials and the subsequent thickening of the wall often significantly compromise the residual lumen leading to ischaemic events distal to the arterial stenosis. However, these initial fatty streak lesions may also evolve into vulnerable plaques susceptible to rupture or erosion. Plaque disruption initiates both platelet adhesion and aggregation on the exposed vascular surface and the activation of the clotting cascade leading to the so-called atherothrombotic process. Yet, platelets have also been shown to be transporters of regulatory molecules (micro-RNA), to drive the inflammatory response and mediate atherosclerosis progression. Here we discuss our current understanding of the pathophysiological mechanisms involved in atherogenesis - from fatty streaks to complex and vulnerable atheromas - and highlight the molecular machinery used by platelets to regulate the atherogenic process, thrombosis and its clinical implications.
动脉粥样硬化是几乎所有冠状动脉疾病和外周动脉疾病以及许多中风病例的根本原因。动脉粥样硬化是一种全身性炎症过程，其特征是在大动脉内膜中脂质和巨噬细胞/淋巴细胞的积累。这些血液来源物质的沉积以及随后的管壁增厚常常严重损害残余腔，导致动脉狭窄远端的缺血事件。然而，这些最初的脂肪条纹病变也可能演变成易破裂或侵蚀的脆弱斑块。斑块破裂启动暴露的血管表面上的血小板黏附和聚集以及凝血级联的激活，导致所谓的动脉粥样血栓形成过程。然而，血小板也被证明是调节分子（micro-RNA）的转运器，以驱动炎症反应并介导动脉粥样硬化的进展。在这里，我们讨论了我们对从脂肪条纹到复杂和脆弱的动脉粥样瘤的动脉粥样硬化形成过程中涉及的病理生理机制的理解，并强调了血小板用于调节动脉粥样硬化形成、血栓形成及其临床意义的分子机制。
