Athrosclerosis is conceived as a chronic inflammatory status affecting cells from vascular walls. Different mechanisms and pathological features are evident at the onset of atherosclerotic changes via the engaging different cells from the vascular wall and circulatory cells. Attempts are currently focused on the detection of cell compensatory mechanisms against atherosclerotic changes to restore cell function and/or postpone severe vasculitis. Autophagy is an intracellular self-digesting process commonly protrudes exhausted organelles and injured cytoplasmic constituents via double-lipid bilayer membrane vesicles out the target cells. Recent investigations point to the critical and defensive role of autophagy in the vascular cells behavioral function such as endothelial cells and smooth muscle cells against different insults. Autophagy response and related effectors could be modulated in the favor to restore cell function and reduce pro-inflammatory status under pathological conditions. In this review, the recent findings were collected regarding the role of autophagy during atherosclerotic changes. We aimed to answer the question of how autophagy stimulation and/or inhibition could provide a promising effect on developing a sophisticated treatment for AS.

中文翻译：

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自噬在动脉粥样硬化中的作用：是敌人还是朋友？

动脉粥样硬化被认为​​是影响血管壁细胞的慢性炎症状态。通过接合来自血管壁和循环细胞的不同细胞，在动脉粥样硬化改变开始时，不同的机制和病理特征是明显的。当前的尝试集中在检测针对动脉粥样硬化变化的细胞补偿机制以恢复细胞功能和/或推迟严重血管炎。自噬是一种细胞内自我消化过程，通常通过双脂质双层膜囊泡将精疲力竭的细胞器和受损的细胞质成分伸出靶细胞。最近的研究指出自噬在血管细胞行为功能中的关键和防御作用，例如内皮细胞和平滑肌细胞针对不同的损伤。可以调节自噬反应和相关效应子，以恢复病理状态下的细胞功能并减少促炎状态。在这篇综述中，收集了有关自噬在动脉粥样硬化改变中的作用的最新发现。我们旨在回答自噬刺激和/或抑制如何为开发AS的复杂治疗方法提供有希望的效果的问题。