Journal
RHEUMATOLOGY
Volume 48, Issue -, Pages 3-7Publisher
OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/ken481
Keywords
Endothelial cell; Endothelin-1; Vasculopathy; Fibrosis; Scleroderma
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The aetiology of SSc is subject to ongoing research, as the precise events that underlie the development of this disease remain unclear. The pathogenesis is known to involve endothelium, epithelium, fibroblasts, innate and adaptive immune systems and their component immunological mediators. Endothelial cell damage may be the initiating factor, but the precise triggering event(s) remain elusive. Angiogenesis also appears to be dysregulated. Vasculopathy shows similarities in different organs (e.g. pulmonary arterial hypertension, renal disease, digital tip ulcers). Endothelin-1 is a potent mediator of vasculopathy, and hence represents a highly relevant target for intervention of vascular features in SSc.
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