Perrotta Ida, Aquila Saveria
Department of Biology, Ecology and Earth Sciences (Di.B.E.S.T.), Transmission Electron Microscopy Laboratory, Centre for Microscopy and Microanalysis (CM2), University of Calabria, 87036 Rende, Italy.
Department of Pharmacy and Sciences of Health and Nutrition, University of Calabria, 87036 Rende, Italy.
Oxid Med Cell Longev. 2015;2015:130315. doi: 10.1155/2015/130315. Epub 2015 Mar 18.
Atherosclerosis is a multifactorial, multistep disorder of large- and medium-sized arteries involving, in addition to age, gender and menopausal status, a complex interplay between lifestyle and genetic risk factors. Atherosclerosis usually begins with the diffusion and retention of atherogenic lipoproteins into the subendothelial space of the artery wall where they become oxidized by local enzymes and accumulate, leading to the formation of a cushion called atheroma or atheromatous or fibrofatty plaque, composed of a mixture of macrophages, lymphocytes, smooth muscle cells (SMCs), cholesterol cleft, necrotic debris, and lipid-laden foam cells. The pathogenesis of atherosclerosis still remains incompletely understood but emerging evidence suggests that it may involve multiple cellular events, including endothelial cell (EC) dysfunction, inflammation, proliferation of vascular SMCs, matrix (ECM) alteration, and neovascularization. Actually, a growing body of evidence indicates that autophagy along with the chronic and acute overproduction of reactive oxygen species (ROS) is integral to the development and progression of the disease and may represent fruitful avenues for biological investigation and for the identification of new therapeutic targets. In this review, we give an overview of ROS and autophagy in atherosclerosis as background to understand their potential role in this vascular disease.
动脉粥样硬化是一种累及大中动脉的多因素、多步骤疾病，除年龄、性别和绝经状态外，还涉及生活方式和遗传风险因素之间的复杂相互作用。动脉粥样硬化通常始于致动脉粥样硬化脂蛋白扩散并滞留于动脉壁的内皮下间隙，在那里它们被局部酶氧化并积聚，导致形成一种称为粥样瘤或粥样或纤维脂肪斑块的垫层，其由巨噬细胞、淋巴细胞、平滑肌细胞（SMC）、胆固醇裂隙、坏死碎片和富含脂质的泡沫细胞混合组成。动脉粥样硬化的发病机制仍未完全阐明，但新出现的证据表明，它可能涉及多个细胞事件，包括内皮细胞（EC）功能障碍、炎症、血管SMC增殖、基质（ECM）改变和新血管形成。实际上，越来越多的证据表明，自噬以及活性氧（ROS）的慢性和急性过度产生是该疾病发生和发展所不可或缺的，并且可能为生物学研究和新治疗靶点的识别提供富有成果的途径。在本综述中，我们概述了动脉粥样硬化中的ROS和自噬，以此作为了解它们在这种血管疾病中潜在作用的背景知识。
