Cell Death in the Vessel Wall: The Good, the Bad, the Ugly.
Cell Death in the Vessel Wall: The Good, the Bad, the Ugly.
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DOI：
10.1161/atvbaha.117.309229
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发表时间：
2017-07
期刊：
影响因子：
--
通讯作者：
Rayner KJ
中科院分区：
文献类型：
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作者：
Rayner KJ
动脉粥样硬化性血管疾病是由新内膜空间中炎症和血管细胞积聚和清除不平衡引起的。当促进细胞募集、存活和增殖的途径优于激活细胞死亡、流出和清除的途径时，斑块就会扩张。相反，程序性细胞死亡和通过胞吞作用有效清除凋亡小体可减少病变细胞结构并促进修复环境和病变稳定性。然而，如果这些精心平衡的途径受到干扰，病变就会积聚细胞碎片、受损的相关分子模式和停滞的巨噬细胞，所有这些都会导致促炎环境和病变不稳定。在这里，我们将回顾对血管壁细胞死亡如何直接协调动脉粥样硬化发展以及哪些分子信号正在协调这些途径的最新理解。我们将讨论细胞死亡的必要性，以及不同形式的细胞死亡的执行如何在斑块中产生不同的结果，以及如何促进病灶中死细胞的有效清除看起来是一条有前途的治疗途径。
Atherosclerotic vascular disease results from an imbalance of inflammatory and vascular cell accumulation and removal in the neointimal space. When pathways that promote cell recruitment, survival and proliferation are favored over to those that activate cell death, egress and clearance, the plaque expands. In contrast, programmed cell death and the efficient clearance of apoptotic bodies by efferocytosis reduces lesion cellularity and promotes a reparative environment and lesion stability. However, should these carefully balanced pathways become disturbed, lesions can accumulate cell debris, damaged-associated molecular patterns and arrested macrophages, all contributing to the pro-inflammatory environment and lesion instability. Here, we will review the latest understanding of how cell death in the vessel wall directly coordinates the development of atherosclerosis, and what molecular signals are orchestrating these pathways. We will discuss the necessity of cell death, and the ways in which the execution of different forms of cell death can direct different outcomes in the plaque, and how promoting the effective clearance of dead cells from the lesion is looking like a promising therapeutic path forward.