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Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo
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The vascular microenvironment and systemic sclerosis.

Tracy Frech1, Nathan Hatton, Boaz Markewitz

  • 1Division of Rheumatology, Department of Internal Medicine, University of Utah, Salt Lake City, UT 84132, USA.

International Journal of Rheumatology
|September 4, 2010
PubMed
Summary
This summary is machine-generated.

Systemic Sclerosis (SSc) vasculopathy, including Raynaud's phenomenon, may precede fibrosis. The vascular microenvironment, involving cell senescence and progenitor cells, likely dictates the extent of organ damage in SSc.

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Area of Science:

  • Vascular biology and immunology
  • Connective tissue diseases
  • Pathogenesis of Systemic Sclerosis

Background:

  • Systemic Sclerosis (SSc) presents clinically with vasculopathy, such as Raynaud's phenomenon and nail bed capillary changes.
  • This vascular damage is a hallmark of SSc, observed in both limited and diffuse cutaneous forms, and is believed to initiate fibrotic processes.
  • The vascular microenvironment's influence on fibrosis progression and end-organ damage in SSc is increasingly recognized.

Purpose of the Study:

  • To elucidate the mechanisms by which the vascular microenvironment influences the severity of end-organ damage in Systemic Sclerosis (SSc).
  • To highlight the roles of specific cellular components within the vascular microenvironment, including senescent vascular cells, endothelial progenitor cells (EPCs), multipotent mesenchymal stem cells (MSCs), pericytes, and angiogenic monocytes.
  • To underscore the importance of understanding these cellular interactions for advancing SSc treatment strategies.

Main Methods:

  • Review and synthesis of existing literature on vascular pathology in Systemic Sclerosis.
  • Focus on cellular and molecular mechanisms within the vascular microenvironment.
  • Analysis of the contributions of endothelial progenitor cells (EPCs), mesenchymal stem cells (MSCs), pericytes, and monocytes to SSc pathogenesis.

Main Results:

  • The vascular microenvironment, characterized by factors like vascular cell senescence, plays a critical role in determining the degree of fibrosis and end-organ damage in SSc.
  • Endothelial progenitor cells (EPCs), multipotent mesenchymal stem cells (MSCs), pericytes, and angiogenic monocytes are key cellular players in SSc vasculopathy and subsequent tissue remodeling.
  • Dysfunction or altered behavior of these vascular cells contributes significantly to the disease's progression.

Conclusions:

  • The vascular microenvironment is a crucial determinant of disease severity and end-organ damage in Systemic Sclerosis (SSc).
  • Targeting cellular components within the vascular microenvironment, such as EPCs, MSCs, pericytes, and monocytes, offers potential therapeutic avenues for SSc.
  • Further research into the vascular microenvironment's role in SSc pathogenesis may lead to more effective and directed treatments.