Institute of Cellular Biology and Pathology Nicolae Simionescu, Romanian Academy, Bucharest, Romania.
J Cell Mol Med. 2012 Sep;16(9):1978-90. doi: 10.1111/j.1582-4934.2012.01552.x.
Sound data support the concept that in atherosclerosis, inflammation and dyslipidemia intersect each other and that irrespective of the initiator, both participate from the early stages to the ultimate fate of the atheromatous plaque. The two partakers manoeuvre a vicious circle in atheroma formation: dyslipidaemia triggers an inflammatory process and inflammation elicits dyslipidaemia. Independent of the initial cause, the atherosclerotic lesions occur focally, in particular arterial-susceptible sites, by a process that, although continuous, can be arbitrarily divided into a sequence of consecutive stages that lead from fatty streak to the fibro-lipid plaque and ultimately to plaque rupture and thrombosis. In the process, the initial event is a change in endothelial cells (EC) constitutive properties. Then, the molecular alarm signals send by dysfunctional EC are decoded by specific blood immune cells (monocytes, T lymphocytes, neutrophils, mast cells) and by the resident vascular cells, that respond by initiating a robust inflammatory process, in which the cells and the factors they secrete hasten the atheroma development. Direct and indirect crosstalk between the cells housed within the nascent plaque, complemented by the increase in risk factors of atherosclerosis lead to atheroma development and outcome. The initial inflammatory response can be regarded as a defense/protective reaction mechanism, but its further amplification, speeds up atherosclerosis. In this review, we provide an overview on the role of inflammation and dyslipidaemia and their intersection in atherogenesis. The data may add to the foundation of a novel attitude in the diagnosis and treatment of atherosclerosis.
声频数据支持以下观点，即在动脉粥样硬化中，炎症和血脂异常相互交叉，并且无论启动因素如何，两者都从动脉粥样斑块的早期阶段参与到最终结局。这两个参与者在动脉粥样斑块形成中操纵一个恶性循环：血脂异常引发炎症过程，炎症又引起血脂异常。无论最初的原因如何，动脉粥样硬化病变都是局部发生的，特别是在动脉易感性部位，这一过程虽然是连续的，但可以任意分为一系列连续的阶段，从脂肪条纹发展到纤维脂质斑块，最终导致斑块破裂和血栓形成。在此过程中，最初的事件是内皮细胞（EC）组成性质的改变。然后，功能失调的 EC 发出的分子报警信号被特定的血液免疫细胞（单核细胞、T 淋巴细胞、中性粒细胞、肥大细胞）和驻留血管细胞解码，这些细胞通过启动强大的炎症过程做出反应，其中细胞及其分泌的因子加速了动脉粥样硬化的发展。新生斑块内细胞的直接和间接串扰，加上动脉粥样硬化风险因素的增加，导致了动脉粥样硬化的发展和结局。最初的炎症反应可以被视为一种防御/保护反应机制，但它的进一步放大加速了动脉粥样硬化的进程。在这篇综述中，我们概述了炎症和血脂异常及其在动脉粥样发生中的相互作用的作用。这些数据可能为动脉粥样硬化的诊断和治疗提供新的思路。
