Apolipoprotein E and Atherosclerosis: From Lipoprotein Metabolism to MicroRNA Control of Inflammation.
Apolipoprotein E and Atherosclerosis: From Lipoprotein Metabolism to MicroRNA Control of Inflammation.
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DOI：
10.3390/jcdd5020030
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发表时间：
2018-05-23
影响因子：
2.4
通讯作者：
Raffai RL
中科院分区：
文献类型：
--
作者：
Bouchareychas L;Raffai RL
载脂蛋白E在血浆载脂蛋白中具有前所未有的抗动脉粥样硬化能力。虽然最好的认识，其能力，介导血浆脂蛋白清除在肝脏和防止巨噬细胞泡沫细胞的形成，我们最近的理解，apoE可以发挥控制动脉粥样硬化的影响已经显着扩大。新发现的apoE的动脉粥样硬化保护特性包括控制高脂血症小鼠过度造血、血液单核细胞活化和主动脉硬化的能力。负责这些令人兴奋的新特性的机制超出了apoE防止细胞脂质过剩的能力。相反，新的发现揭示了apoE在调节免疫系统和血管壁细胞中microRNA控制的细胞信号传导中的作用。值得注意的是，输注apoE响应性microRNA模拟物显示出在保护患有高脂血症的小鼠免受全身和血管炎症以抑制动脉粥样硬化方面替代apoE。最后，最近的证据表明，apoE可以控制微泡的释放，微泡可以远距离调节细胞信号传导、炎症和动脉粥样硬化。这些令人兴奋的新发现将apoE定位于新兴的细胞间通讯领域，这可能为控制动脉粥样硬化性心血管疾病引入新的方法。
Apolipoprotein (apo) E stands out among plasma apolipoproteins through its unprecedented ability to protect against atherosclerosis. Although best recognized for its ability to mediate plasma lipoprotein clearance in the liver and protect against macrophage foam cell formation, our recent understanding of the influence that apoE can exert to control atherosclerosis has significantly widened. Among apoE’s newfound athero-protective properties include an ability to control exaggerated hematopoiesis, blood monocyte activation and aortic stiffening in mice with hyperlipidemia. Mechanisms responsible for these exciting new properties extend beyond apoE’s ability to prevent cellular lipid excess. Rather, new findings have revealed a role for apoE in regulating microRNA-controlled cellular signaling in cells of the immune system and vascular wall. Remarkably, infusions of apoE-responsive microRNA mimics were shown to substitute for apoE in protecting against systemic and vascular inflammation to suppress atherosclerosis in mice with hyperlipidemia. Finally, more recent evidence suggests that apoE may control the release of microvesicles that could modulate cellular signaling, inflammation and atherosclerosis at a distance. These exciting new findings position apoE within the emerging field of intercellular communication that could introduce new approaches to control atherosclerosis cardiovascular disease.
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影响因子：
4.4
作者：
Adamson S;Leitinger N
通讯作者：
Leitinger N
影响因子：
11.1
作者：
Cheng, Henry S.;Sivachandran, Nirojini;Lau, Andrew;Boudreau, Emilie;Zhao, Jimmy L.;Baltimore, David;Delgado-Olguin, Paul;Cybulsky, Myron I.;Fish, Jason E.
通讯作者：
Fish, Jason E.
影响因子：
6.5
作者：
Getz, Godfrey S.;Reardon, Catherine A.
通讯作者：
Reardon, Catherine A.
具有遗传转换的高脂血症的逆转会影响动脉粥样硬化斑块中巨噬细胞的含量和炎症状态。
影响因子：
37.8
作者：
Feig JE;Parathath S;Rong JX;Mick SL;Vengrenyuk Y;Grauer L;Young SG;Fisher EA
通讯作者：
Fisher EA
DOI：
10.1161/atvbaha.112.246389
发表时间：
2012-05-01
影响因子：
8.7
作者：
Eberle, Delphine;Kim, Roy Y.;Raffai, Robert L.
通讯作者：
Raffai, Robert L.