Macrophage apoptosis in atherosclerosis: consequences on plaque progression and the role of endoplasmic reticulum stress.
Macrophage apoptosis in atherosclerosis: consequences on plaque progression and the role of endoplasmic reticulum stress.
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DOI：
10.1089/ars.2009.2469
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发表时间：
2009-09
影响因子：
6.6
通讯作者：
Tabas I
中科院分区：
文献类型：
--
作者：
Tabas I
动脉粥样硬化血栓性血管疾病，如心肌梗塞和中风，是工业化国家的主要死亡原因。这些疾病的直接原因是供应关键器官的中型动脉中的急性闭塞性血栓形成。血栓形成是由少数动脉粥样硬化斑块的破裂或侵蚀引发的，这些斑块已经发展到特定的“易损性”阶段。“脆弱斑块的特征是某些关键特征，如炎症，保护性胶原帽变薄，以及由巨噬细胞碎片组成的富含脂质的坏死核心。许多细胞事件导致易损斑块形成，包括巨噬细胞分泌促炎、促凝血和蛋白水解分子，以及巨噬细胞、内膜平滑肌细胞和可能的内皮细胞死亡。尤其是坏死核心是斑块脆弱性的关键因素，因为巨噬细胞碎片促进炎症、斑块不稳定和血栓形成。斑块坏死是由病变巨噬细胞凋亡和这些死细胞的清除缺陷（称为巨噬细胞增多症）的组合引起的。这篇评论将集中在如何巨噬细胞凋亡，在设置有缺陷的巨噬细胞，有助于坏死核心的形成和如何一个过程中已知的是突出的先进病变激活ER应激信号转导通路，有助于巨噬细胞凋亡在这些斑块。
Atherothrombotic vascular diseases, such as myocardial infraction and stroke, are the leading cause of death in the industrialized world. The immediate cause of these diseases is acute occlusive thrombosis in medium-sized arteries feeding critical organs. Thrombosis is triggered by the rupture or erosion of a minority of atherosclerotic plaques that have advanced to a particular stage of "ulnerability." Vulnerable plaques are characterized by certain key features, such as inflammation, thinning of a protective collagenous cap, and a lipid-rich necrotic core consisting of macrophage debris. A number of cellular events contribute to vulnerable plaque formation, including secretion of pro-inflammatory, pro-coagulant, and proteolytic molecules by macrophages as well as death of macrophages, intimal smooth muscles cells, and possibly endothelial cells. The necrotic core in particular is a key factor in plaque vulnerability, because the macrophage debris promotes inflammation, plaque instability, and thrombosis. Plaque necrosis arises from a combination of lesional macrophage apoptosis and defective clearance of these dead cells, a process called efferocytosis. This review will focus on how macrophage apoptosis, in the setting of defective efferocytosis, contributes to necrotic core formation and how a process known to be prominent in advanced lesions—activation of ER stress signal transduction pathways—contributes to macrophage apoptosis in these plaques.
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影响因子：
15.9
作者：
Fadok, VA;Bratton, DL;Henson, PM
通讯作者：
Henson, PM
影响因子：
24
作者：
Imoto, K;Hiro, T;Matsuzaki, M
通讯作者：
Matsuzaki, M
DOI：
10.1073/pnas.1732494100
发表时间：
2003-09-02
影响因子：
11.1
作者：
Feng, B;Zhang, DJ;Tabas, I
通讯作者：
Tabas, I
影响因子：
21.3
作者：
Feng, B;Yao, PM;Tabas, I
通讯作者：
Tabas, I
影响因子：
4.8
作者：
Li, YK;Ge, MT;Tabas, I
通讯作者：
Tabas, I