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Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
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Jugular Venous Pressure (JVP) Measurement
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Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease
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Is scleroderma a vasculopathy?

Jo Nadine Fleming1, Richard A Nash, William M Mahoney

  • 1University of Washington School of Medicine, 815 Mercer Street, #419, Brotman Building, Seattle, WA 98109, USA. flemij@u.washington.edu

Current Rheumatology Reports
|March 20, 2009
PubMed
Summary
This summary is machine-generated.

Scleroderma, an autoimmune disease, is characterized by systemic vasculopathy, including noninflammatory vascular changes and thickened neointima. This study hypothesizes vascular injury is central to scleroderma, suggesting potential clinical interventions.

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A Methodological Approach to Non-invasive Assessments of Vascular Function and Morphology
09:33

A Methodological Approach to Non-invasive Assessments of Vascular Function and Morphology

Published on: February 7, 2015

Area of Science:

  • Autoimmune diseases
  • Vascular biology
  • Connective tissue disorders

Background:

  • Scleroderma is an autoimmune collagen vascular disease.
  • A key feature is systemic vasculopathy with noninflammatory macrovascular and microvascular changes.
  • Characteristic changes include thickened neointima and an unusual endothelial cell phenotype.

Purpose of the Study:

  • To investigate the role of vascular injury in scleroderma.
  • To understand the endothelial cell phenotype in scleroderma.
  • To propose potential clinical strategies for managing scleroderma.

Main Methods:

  • Analysis of vascular changes in scleroderma.
  • Examination of endothelial cell markers, including vascular endothelial (VE)-cadherin.
  • Assessment of gene expression related to vascular rarefaction, such as type 1 interferon and regulator of G protein signaling 5 (RGS5).

Main Results:

  • Scleroderma exhibits noninflammatory vascular changes and thickened neointima.
  • Endothelial cells show loss of VE-cadherin and express type 1 interferon and RGS5.
  • Hypoxia and high vascular endothelial growth factor (VEGF) levels are observed, particularly early in the disease.

Conclusions:

  • Vascular injury is hypothesized to be central to the pathogenesis of scleroderma.
  • The combination of VEGF and rarefaction, along with interferon and RGS5 expression, suggests complex vascular dynamics.
  • Potential clinical approaches to arrest or reverse scleroderma progression are proposed based on these findings.