Macrophages play a central role in the development of atherosclerotic cardiovascular disease (ASCVD), which encompasses coronary artery disease, peripheral artery disease, cerebrovascular disease, and aortic atherosclerosis. In each vascular bed, macrophages contribute to the maintenance of the local inflammatory response, propagate plaque development, and promote thrombosis. These central roles, coupled with their plasticity, makes macrophages attractive therapeutic targets in stemming the development of and stabilizing existing atherosclerosis. In the context of ASCVD, classically activated M1 macrophages initiate and sustain inflammation, and alternatively activated M2 macrophages resolve inflammation. However, this classification is now considered an oversimplification, and a greater understanding of plaque macrophage physiology in ASCVD is required to aid in the development of therapeutics to promote ASCVD regression. Reviewed herein are the macrophage phenotypes and molecular regulators characteristic of ASCVD regression, and the current murine models of ASCVD regression.

中文翻译：

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巨噬细胞在动脉粥样硬化回归中。

巨噬细胞在动脉粥样硬化性心血管疾病（ASCVD）的发展中起着核心作用，其中包括冠状动脉疾病，外周动脉疾病，脑血管疾病和主动脉粥样硬化。在每个血管床中，巨噬细胞有助于维持局部炎症反应，传播斑块发育并促进血栓形成。这些主要作用及其可塑性使巨噬细胞成为阻止和发展现有动脉粥样硬化发展的有吸引力的治疗靶标。在ASCVD的背景下，经典激活的M1巨噬细胞引发并维持炎症，或者可选地，激活的M2巨噬细胞解决炎症。但是，现在将这种分类视为过分简化，并且需要对ASCVD中的斑块巨噬细胞生理有更多的了解，以帮助开发促进ASCVD消退的疗法。本文审查的是ASCVD回归的巨噬细胞表型和分子调节剂的特征，以及ASCVD回归的当前鼠模型。