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Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

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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 but also impacts other areas, such as the arms, thereby impairing overall circulation and organ function.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty deposits inside the arterial...
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Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
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Updated: Jul 15, 2025

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
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Endothelial Dysfunction in Systemic Sclerosis.

Eshaan Patnaik1, Matthew Lyons2, Kimberly Tran2

  • 1Department of Biology, Memphis University School, Memphis, TN 38119, USA.

International Journal of Molecular Sciences
|September 28, 2023
PubMed
Summary
This summary is machine-generated.

Systemic sclerosis, or scleroderma, is an autoimmune disease where vascular dysfunction is a primary event. This review explores the molecular mechanisms of endothelial dysfunction in scleroderma pathogenesis.

Keywords:
angiogenesisendothelial cellsystemic sclerosisvasculogenesis

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Area of Science:

  • Immunology
  • Vascular Biology
  • Fibrosis Research

Background:

  • Systemic sclerosis (Scleroderma) is an autoimmune disease characterized by vascular issues, autoimmunity, and fibrosis.
  • Raynaud phenomenon and skin thickening are common manifestations, suggesting vascular dysfunction precedes fibrosis.
  • The precise cause is unknown but involves environmental triggers in genetically susceptible individuals.

Purpose of the Study:

  • To review the molecular mechanisms underlying endothelial dysfunction in systemic sclerosis.
  • To highlight the role of endothelial damage and activation in disease development.
  • To discuss endothelial to mesenchymal cell transformation in fibrosis.

Main Methods:

  • Literature review focusing on molecular and cellular aspects of endothelial dysfunction.
  • Analysis of studies on vascular abnormalities, autoimmunity, and fibrosis in systemic sclerosis.
  • Examination of endothelial progenitor cell function and angiogenesis defects.

Main Results:

  • Endothelial damage and activation are early events, potentially triggered by infections and autoantibodies.
  • Defects in endothelial progenitor cells contribute to impaired angiogenesis and vasculogenesis.
  • Endothelial to mesenchymal cell transformation is a key process in systemic sclerosis pathogenesis.

Conclusions:

  • Endothelial dysfunction is a critical factor in the development of systemic sclerosis.
  • Understanding these molecular pathways may lead to targeted therapies for scleroderma.
  • Further research into endothelial cell biology is essential for managing this complex disease.