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Updated: Apr 8, 2026

A Model of Disturbed Flow-Induced Atherosclerosis in Mouse Carotid Artery by Partial Ligation and a Simple Method of RNA Isolation from Carotid Endothelium
11:00

A Model of Disturbed Flow-Induced Atherosclerosis in Mouse Carotid Artery by Partial Ligation and a Simple Method of RNA Isolation from Carotid Endothelium

Published on: June 23, 2010

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ApoE controls the interface linking lipids and inflammation in atherosclerosis

Christian Weber1, Oliver Soehnlein

  • 1Institute for Cardiovascular Prevention, Ludwig-Maximilians-University Munich, Munich, Germany. christian.weber@med.uni-muenchen.de

The Journal of Clinical Investigation
|October 5, 2011
PubMed

Insights

High cholesterol (hypercholesterolemia) and high white blood cell counts (leukocytosis) contribute to atherosclerosis. A new study reveals a mechanistic link between these factors, offering potential new treatments for arterial disease.

Area of Science:

  • Cardiovascular Science
  • Immunology
  • Pathology

Background:

  • Atherosclerosis is a chronic inflammatory arterial disease.
  • Hypercholesterolemia and leukocytosis are independent risk factors.
  • Arterial leukocyte infiltration contributes to disease progression.

Purpose of the Study:

  • To identify a mechanistic link between hypercholesterolemia and leukocytosis in atherosclerosis.
  • To investigate the role of leukocyte homeostasis in atherosclerotic lesion development.

Main Methods:

  • The study utilized a mouse model to investigate the relationship between hypercholesterolemia and leukocytosis.
  • Mechanistic pathways connecting these conditions and lesion development were explored.

Main Results:

  • Murphy and colleagues identified a mechanistic link between hypercholesterolemia and leukocytosis.
  • This link promotes arterial leukocyte infiltration and atherosclerotic lesion formation in mice.

Conclusions:

  • Hypercholesterolemia and leukocytosis are mechanistically linked in the development of atherosclerosis.
  • Findings suggest novel therapeutic strategies targeting leukocyte homeostasis to manage atherosclerosis.

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