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Angiogenesis and vasculogenesis in systemic sclerosis

J H W Distler1, S Gay, O Distler

  • 1Department of Internal Medicine III, University of Erlangen-Nuremberg, Germany.

Rheumatology (Oxford, England)
|September 22, 2006
PubMed

Insights

Systemic sclerosis (SSc) involves vascular damage and impaired blood vessel formation. Paradoxical vascular endothelial growth factor (VEGF) overexpression in SSc may contribute to abnormal vessel development, despite its potential to heal ulcers.

Area of Science:

  • Rheumatology
  • Vascular Biology
  • Pathogenesis of Systemic Sclerosis

Background:

  • Systemic sclerosis (SSc) is characterized by vascular changes, inflammation, and extracellular matrix accumulation.
  • Endothelial cell apoptosis and damage markers are elevated in SSc patients.
  • Despite insufficient angiogenesis, vascular endothelial growth factor (VEGF) is overexpressed in SSc.

Purpose of the Study:

  • To investigate the role of vascular endothelial growth factor (VEGF) in the pathogenesis of systemic sclerosis (SSc).
  • To explore the paradoxical effects of VEGF overexpression on vascular development in SSc.
  • To examine the contribution of impaired vasculogenesis and endothelial progenitor cells to SSc vascular defects.

Main Methods:

  • Analysis of endothelial cell apoptosis markers in SSc patients.
  • Assessment of vascular endothelial growth factor (VEGF) levels and its correlation with angiogenesis.
  • Evaluation of endothelial progenitor cell number and function in SSc.

Main Results:

  • Elevated markers of endothelial cell damage and apoptosis in SSc.
  • Overexpression of vascular endothelial growth factor (VEGF) in SSc patients.
  • Paradoxical effects of prolonged VEGF overexpression leading to irregular vessel formation.
  • Impaired vasculogenesis due to reduced and functionally deficient endothelial progenitor cells in SSc.

Conclusions:

  • Vascular changes, including impaired angiogenesis and vasculogenesis, are central to SSc pathogenesis.
  • Overexpressed VEGF in SSc may paradoxically promote abnormal vascular remodeling rather than effective angiogenesis.
  • Defects in endothelial progenitor cells further contribute to the vascular complications observed in SSc.

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