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Am J Physiol Heart Circ Physiol. 2017 Mar 1;312(3):H349-H354. doi: 10.1152/ajpheart.00759.2016. Epub 2016 Dec 16.

A pathogenic role of complement in arterial hypertension and hypertensive end organ damage.

Author information

1
Department of Medicine, University Hospital Hamburg-Eppendorf, Hamburg, Germany; wenzel@uke.de.
2
German Centre for Cardiovascular Research (DZHK), partner site Hamburg/Kiel/Lübeck, Germany.
3
Department of Medicine, University Hospital Hamburg-Eppendorf, Hamburg, Germany.
4
Institute for Systemic Inflammation Research, Lübeck, Germany.
5
Division of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
6
Department of Cellular and Integrative Physiology, University Hospital Hamburg-Eppendorf, Hamburg, Germany; and.

Abstract

The self-amplifying cascade of messenger and effector molecules of the complement system serves as a powerful danger-sensing system that protects the host from a hostile microbial environment, while maintaining proper tissue and organ function through effective clearance of altered or dying cells. As an important effector arm of innate immunity, it also plays important roles in the regulation of adaptive immunity. Innate and adaptive immune responses have been identified as crucial players in the pathogenesis of arterial hypertension and hypertensive end organ damage. In line with this view, complement activation may drive the pathology of hypertension and hypertensive injury through its impact on innate and adaptive immune responses. It is well known that complement activation can cause tissue inflammation and injury and complement-inhibitory drugs are effective treatments for several inflammatory diseases. In addition to these proinflammatory properties, complement cleavage fragments of C3 and C5 can exert anti-inflammatory effects that dampen the inflammatory response to injury. Recent experimental data strongly support a role for complement in arterial hypertension. The remarkably similar clinical and histopathological features of malignant nephrosclerosis and atypical hemolytic uremic syndrome, which is driven by complement activation, suggest a role for complement also in the development of malignant nephrosclerosis. Herein, we will review canonical and noncanonical pathways of complement activation as the framework to understand the multiple roles of complement in arterial hypertension and hypertensive end organ damage.

KEYWORDS:

C1q; C3aR; C5aR1; C5aR2; arterial hypertension; complosome

PMID:
27986662
DOI:
10.1152/ajpheart.00759.2016
[Indexed for MEDLINE]
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