Journal
CURRENT RHEUMATOLOGY REPORTS
Volume 14, Issue 1, Pages 56-63Publisher
SPRINGER
DOI: 10.1007/s11926-011-0219-1
Keywords
Systemic sclerosis; Scleroderma; Angiogenesis; Vasculopathy; Vasculogenesis; Endothelial cells
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Funding
- National Institutes of Health [HL094017]
- Office of Research and Development, Medical Research Service, Department of Veterans Affairs
- Scleroderma Foundation
- Frederick G. L. Huetwell and William D. Robinson, MD, Professorship in Rheumatology
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Systemic sclerosis (scleroderma [SSc]) is a multifactorial disease characterized by inflammation, extensive and progressive fibrosis, and multiple vasculopathies. The vascular manifestations can be seen early in the pathogenesis of the disease and include malformed capillaries, Raynaud's phenomenon, and digital ulcers. As the disease progresses, the vasculopathy proceeds to significant clinical manifestations, including renal crisis and pulmonary arterial hypertension. Moreover, later stages of the disease are marked by increasingly avascular areas. Despite the obliteration of microvascular structures, compensatory vasculogenesis and angiogenesis do not occur normally. This is in spite of a general increase in many potent angiogenic factors. Recent studies are beginning to examine this paradox and subsequent paucity of an angiogenic response in SSc. In this review, we discuss these findings and examine the role that chemokine and growth factor receptors, proteases, adhesion molecules, and transcription factors play in the dysregulation of angiogenesis in SSc.
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