Document Detail

Overview of pathogenesis of systemic sclerosis.
MedLine Citation:
PMID:  19487220     Owner:  NLM     Status:  MEDLINE    
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.
D J Abraham; T Krieg; J Distler; O Distler
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Rheumatology (Oxford, England)     Volume:  48 Suppl 3     ISSN:  1462-0332     ISO Abbreviation:  Rheumatology (Oxford)     Publication Date:  2009 Jun 
Date Detail:
Created Date:  2009-06-02     Completed Date:  2009-07-06     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100883501     Medline TA:  Rheumatology (Oxford)     Country:  England    
Other Details:
Languages:  eng     Pagination:  iii3-7     Citation Subset:  AIM; IM    
Centre for Rheumatology and Connective Tissue Disease, Royal Free and University College Medical School, University College London, Hampstead, London, UK.
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MeSH Terms
Endothelium, Vascular / immunology,  pathology
Epithelium / immunology,  pathology
Fibroblasts / immunology,  pathology
Lung / immunology,  pathology
Scleroderma, Systemic / etiology*,  immunology
Skin / immunology,  pathology

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