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This article is part of the supplement: Advances in systemic sclerosis and related fibrotic and vascular conditions

Review

Vasculopathy and disordered angiogenesis in selected rheumatic diseases: rheumatoid arthritis and systemic sclerosis

Alisa E Koch1* and Oliver Distler2

Author Affiliations

1 Veterans' Hospital, and the University of Michigan Medical School, Zina Pitcher Place, Ann Arbor, Michigan 48109-2200, USA

2 Center of Experimental Rheumatology/Integrative Human Physiology and Department of Rheumatology, University Hospital Zürich, Gloriastrasse, CH-8091 Zürich, Switzerland

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Arthritis Research & Therapy 2007, 9(Suppl 2):S3  doi:10.1186/ar2187

Published: 15 August 2007

Abstract

Angiogenesis is important in the pathogenesis of systemic inflammatory rheumatic diseases, a family of related disorders that includes rheumatoid arthritis and systemic sclerosis. Rheumatoid arthritis is the rheumatic disease in which the role of angiogenesis has been studied most extensively. However, whereas rheumatoid arthritis is characterized by excessive angiogenesis, the situation is not as clear cut in other rheumatic diseases. For example, systemic sclerosis is characterized by reduced capillary density with insufficient angiogenic responses. Results with angiogenesis inhibitors are controversial, and there is – in parallel – a wide range of upregulated angiogenic factors such as vascular endothelial growth factor. Dysregulation of angiogenesis in systemic sclerosis is accompanied by other pathogenic processes, including fibrosis, autoimmunity and vasculopathy. Animal models with at least partial features of the vasculopathy observed in systemic sclerosis include wound healing models, graft versus host disease models and, in particular, the University of California at Davis line 200 chicken model of systemic sclerosis.