Dorian O Haskard1, Joseph J Boyle, Justin C Mason. 1. Bywaters Centre for Vascular Inflammation, National Heart and Lung Institute, Imperial College, Hammersmith Hospital, London, UK. d.haskard@imperial.ac.uk
Abstract
PURPOSE OF REVIEW: Although it has long been recognized that atherosclerotic lesions show evidence of complement activation, the functional roles of the complement system in atherogenesis are not yet fully resolved. This article highlights recent publications on the complement system in the atherosclerosis field. RECENT FINDINGS: There have been a number of recent papers reporting on the association of complement proteins and complement regulators with high density lipoproteins, complement activation by enzymatically-modified LDL, signalling pathways downstream of C3a and C5a receptors and membrane C5b-9 assembly, and the prevention of C5b-9 assembly on endothelial cells via upregulation of CD59 expression in response to arterial laminar flow. C1q has been found to play a protective role in early lesion formation in LDL receptor deficient mice, and Crry-Ig and soluble C1 inhibitor have both been shown to have therapeutic effects in models of vascular injury in ApoE deficient mice. The possibility that the Y402H Factor H polymorphism influences atherosclerosis has been supported in a recent paper showing increased risk in white hypertensive individuals. SUMMARY: The articles that have emerged over the last year highlight the relevance of the complement system to the atherosclerosis field.
PURPOSE OF REVIEW: Although it has long been recognized that atherosclerotic lesions show evidence of complement activation, the functional roles of the complement system in atherogenesis are not yet fully resolved. This article highlights recent publications on the complement system in the atherosclerosis field. RECENT FINDINGS: There have been a number of recent papers reporting on the association of complement proteins and complement regulators with high density lipoproteins, complement activation by enzymatically-modified LDL, signalling pathways downstream of C3a and C5a receptors and membrane C5b-9 assembly, and the prevention of C5b-9 assembly on endothelial cells via upregulation of CD59 expression in response to arterial laminar flow. C1q has been found to play a protective role in early lesion formation in LDL receptor deficient mice, and Crry-Ig and soluble C1 inhibitor have both been shown to have therapeutic effects in models of vascular injury in ApoE deficient mice. The possibility that the Y402H Factor H polymorphism influences atherosclerosis has been supported in a recent paper showing increased risk in white hypertensive individuals. SUMMARY: The articles that have emerged over the last year highlight the relevance of the complement system to the atherosclerosis field.
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