Vascular inflammatory cells in hypertension.
Vascular inflammatory cells in hypertension.
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DOI：
10.3389/fphys.2012.00128
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发表时间：
2012
影响因子：
4
通讯作者：
Titze JM
中科院分区：
文献类型：
--
作者：
Harrison DG;Marvar PJ;Titze JM
高血压是一种常见的疾病，病因不明。在过去的几年中，先天性和适应性免疫系统的组成部分在高血压中起着重要作用。巨噬细胞和T细胞在高血压患者的血管周围脂肪、心脏和肾脏以及实验性高血压动物中积累。各种免疫抑制剂可降低血压并防止终末器官损伤。缺乏淋巴细胞的小鼠可以防止高血压，过继性转移T细胞而不是B细胞可以恢复它们对血管紧张素II或高盐等刺激的血压反应。最近的研究表明，缺乏巨噬细胞的小鼠对血管紧张素II的反应减弱了高血压，而巨噬细胞的基因缺失显著降低了实验性高血压。树突状细胞也与这种疾病有关。许多高血压刺激对中枢神经系统具有触发作用，并且来自室周器官的信号似乎促进炎症。研究表明，中枢信号激活巨噬细胞和T细胞，巨噬细胞和T细胞归巢肾脏和血管系统并释放细胞因子，包括IL-6和IL-17，这反过来又导致肾脏和血管功能障碍并导致血压升高。这些最新发现为高血压提供了新的认识，并为治疗这一严重疾病提供了新的治疗机会。
Hypertension is a common disorder with uncertain etiology. In the last several years, it has become evident that components of both the innate and adaptive immune system play an essential role in hypertension. Macrophages and T cells accumulate in the perivascular fat, the heart and the kidney of hypertensive patients, and in animals with experimental hypertension. Various immunosuppressive agents lower blood pressure and prevent end-organ damage. Mice lacking lymphocytes are protected against hypertension, and adoptive transfer of T cells, but not B cells in the animals restores their blood pressure response to stimuli such as angiotensin II or high salt. Recent studies have shown that mice lacking macrophages have blunted hypertension in response to angiotensin II and that genetic deletion of macrophages markedly reduces experimental hypertension. Dendritic cells have also been implicated in this disease. Many hypertensive stimuli have triggering effects on the central nervous system and signals arising from the circumventricular organ seem to promote inflammation. Studies have suggested that central signals activate macrophages and T cells, which home to the kidney and vasculature and release cytokines, including IL-6 and IL-17, which in turn cause renal and vascular dysfunction and lead to blood pressure elevation. These recent discoveries provide a new understanding of hypertension and provide novel therapeutic opportunities for treatment of this serious disease.
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影响因子：
37.8
作者：
Kvakan, Heda;Kleinewietfeld, Markus;Muller, Dominik N.
通讯作者：
Muller, Dominik N.
DOI：
10.1152/ajpregu.00645.2006
发表时间：
2007-07-01
影响因子：
2.8
作者：
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通讯作者：
Rodriguez-Iturbe, Bernardo
影响因子：
8.3
作者：
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通讯作者：
Tsugane, S
影响因子：
8.3
作者：
Barhoumi, Tlili;Kasal, Daniel A.;Schiffrin, Ernesto L.
通讯作者：
Schiffrin, Ernesto L.
影响因子：
8.3
作者：
Kasal, Daniel A.;Barhoumi, Tlili;Schiffrin, Ernesto L.
通讯作者：
Schiffrin, Ernesto L.