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Monocyte Recruitment Versus Macrophage Proliferation in Atherosclerosis
Circulation Research ( IF 20.1 ) Pub Date : 2017-10-27 , DOI: 10.1161/circresaha.117.311973
Jenny E Kanter 1
Affiliation  

Atherosclerosis, the underlying pathology in most cardiovascular disease, is a chronic inflammatory disease,1 characterized by accumulation of macrophages in the subendothelial space. Macrophages are protagonists of the disease, both early in the disease as well as during later stages of atherosclerotic lesion progression, with a continuous turnover of the cells.2 Blood monocytes enter the artery wall and differentiate into macrophages, contributing to atherosclerotic lesion growth,3 but local proliferation and survival of existing artery wall macrophages also contribute to lesional macrophage plaque burden (Figure).2 Figure. Macrophages play an important role in all phases of atherosclerosis. Monocyte recruitment is critical during early atherosclerotic disease (and perhaps during certain other situations; left ), and thus at this stage of the disease, blood monocyte levels are an important determining factor. Local macrophage proliferation dominates macrophage accumulation in later stages of atherosclerosis ( right ). Macrophage protein kinase C (PKC) δ is induced by modified lipids that can be found in the plaque. Myeloid cell PKCδ primarily impairs macrophage survival and proliferation, via regulation of phosphorylation of Akt and Foxo3a and ultimately the apoptotic regulator Bim. Deletion knockout (KO) of PKCδ results in increased proliferation and survival, both in the artery wall and in the spleen resulting in more atherosclerosis and enlargement of the spleen. SMC indicates smooth muscle cells. Article, see p …

中文翻译:

动脉粥样硬化中单核细胞募集与巨噬细胞增殖

动脉粥样硬化是大多数心血管疾病的根本病理,是一种慢性炎症性疾病,其特征是巨噬细胞在内皮下间隙积聚。巨噬细胞是疾病的主角,无论是在疾病早期还是在动脉粥样硬化病变进展的后期,细胞都会不断更新。2血液单核细胞进入动脉壁并分化为巨噬细胞,促进动脉粥样硬化病变生长,3但现有动脉壁巨噬细胞的局部增殖和存活也导致病变巨噬细胞斑块负担(图)。2 图。巨噬细胞在动脉粥样硬化的各个阶段都发挥着重要作用。单核细胞的募集在早期动脉粥样硬化疾病期间(也许在某些其他情况下;左图)至关重要,因此在疾病的这个阶段,血液单核细胞水平是一个重要的决定因素。在动脉粥样硬化后期,局部巨噬细胞增殖主导巨噬细胞积累(右)。巨噬细胞蛋白激酶 C (PKC) δ 是由斑块中的修饰脂质诱导的。骨髓细胞 PKCδ 主要通过调节 Akt 和 Foxo3a 的磷酸化以及最终调节凋亡调节因子 Bim 来损害巨噬细胞的存活和增殖。PKCδ 的缺失敲除 (KO) 会导致动脉壁和脾脏中的增殖和存活增加,从而导致更多的动脉粥样硬化和脾脏肿大。SMC表示平滑肌细胞。文章,参见第...
更新日期:2017-10-27
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