The role of complement in arterial hypertension and hypertensive end organ damage

被引:36
作者
Wenzel, Ulrich O. [1 ]
Kemper, Claudia [2 ,3 ]
Bode, Marlies [1 ]
机构
[1] Univ Hosp Hamburg Eppendorf, Dept Med 3, Martinistr 52, D-20246 Hamburg, Germany
[2] NHLBI, Complement & Inflammat Res Sect CIRS, NIH, Bldg 10, Bethesda, MD 20892 USA
[3] Univ Lubeck, Inst Syst Inflammat Res, Lubeck, Germany
关键词
arterial hypertension; atypical hemolytic uremic syndrome; C5aR1; C5aR2; C3aR; C3; C1q; malignantnephrosclerosis; II-INDUCED HYPERTENSION; L CTSL1 PROMOTER; T-CELL; CONCISE GUIDE; THROMBOTIC MICROANGIOPATHY; INTRACELLULAR COMPLEMENT; C5A RECEPTOR; RENAL INJURY; C3; INFLAMMATION;
D O I
10.1111/bph.15171
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Increasing evidence indicates that hypertension and hypertensive end organ damage are not only mediated by haemodynamic injury but that inflammation also plays an important role. The complement system protects the host from a hostile microbial environment and maintains tissue and cell integrity through the elimination of altered or dead cells. As an important effector arm of innate immunity, it plays also central roles in the regulation of adaptive immunity. Thus, complement activation may drive the pathology of hypertension through its effects on innate and adaptive immune responses, aside from direct effects on the vasculature. Recent experimental data strongly support a role for complement in all stages of arterial hypertension. The remarkably similar clinical and histopathological features of malignant nephrosclerosis and atypical haemolytic uraemic syndrome suggest also a role for complement in the development of malignant nephrosclerosis. Here, we review the role of complement in hypertension and hypertensive end organ damage.
引用
收藏
页码:2849 / 2862
页数:14
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