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Related Concept Videos

Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

654
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...
654

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Related Experiment Video

Updated: Apr 24, 2026

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
06:35

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Published on: April 27, 2016

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Endothelial dysfunction in systemic sclerosis.

Nezam Altorok1, Yongqing Wang, Bashar Kahaleh

  • 1Division of Rheumatology and Immunology, Department of Internal Medicine, University of Toledo Medical Center, Toledo, Ohio, USA.

Current Opinion in Rheumatology
|September 6, 2014
PubMed
Summary
This summary is machine-generated.

Microvascular endothelial cells (MVECs) dysfunction is central to systemic sclerosis (SSc) pathogenesis. Recent findings reveal MVEC injury impacts fibroblast activation and involves epigenetic factors, anti-endothelial antibodies, and growth factor signaling defects.

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Last Updated: Apr 24, 2026

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Area of Science:

  • Vascular Biology
  • Immunology
  • Rheumatology

Background:

  • Microvascular endothelial cells (MVECs) injury is an early event in systemic sclerosis (SSc) pathogenesis.
  • Understanding MVEC dysfunction is crucial for SSc research.

Purpose of the Study:

  • To update on the role of MVECs in SSc pathogenesis.
  • To elucidate mechanisms of MVEC dysfunction in SSc.

Main Methods:

  • Review of recent scientific literature.
  • Analysis of emerging evidence on MVEC injury mechanisms in SSc.

Main Results:

  • MVECs play a central role in SSc, beyond vascular disease initiation.
  • MVEC dysfunction contributes to fibroblast activation via cytokines and growth factors.
  • Epigenetic factors, progenitor cell defects, anti-endothelial antibodies (e.g., anti-ICAM-1), and impaired VEGF signaling are implicated in SSc pathogenesis.

Conclusions:

  • MVEC dysfunction is a key pathogenic element in SSc.
  • The initial triggers for MVEC dysfunction in SSc remain unidentified.