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Implantation of a Carotid Cuff for Triggering Shear-stress Induced Atherosclerosis in Mice
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The development and progression of atherosclerosis: evidence supporting a role for endoplasmic reticulum (ER) stress

Cameron S McAlpine1, Geoff H Werstuck

  • 1Thrombosis and Atherosclerosis Research Institute, 237 Barton Street East, Hamilton, Ontario, Canada L8L 2X2.

Cardiovascular & Hematological Disorders Drug Targets
|August 31, 2013
PubMed

Insights

Endoplasmic reticulum (ER) stress, a cellular dysfunction, is increasingly linked to atherosclerosis, the main cause of cardiovascular disease. Targeting ER stress may offer new therapeutic strategies for preventing and treating this widespread condition.

Area of Science:

  • Cardiovascular biology
  • Cellular stress response
  • Molecular medicine

Background:

  • Cardiovascular disease (CVD) remains the leading global cause of mortality.
  • Atherosclerosis, a chronic inflammatory arterial disease, underlies most CVD cases.
  • Current understanding of molecular links between risk factors and atherosclerosis progression is incomplete.

Purpose of the Study:

  • To review the role of endoplasmic reticulum (ER) stress in atherosclerosis.
  • To explore ER stress involvement in the initiation and progression of the disease.
  • To discuss potential therapeutic strategies targeting ER stress for anti-atherogenic treatments.

Main Methods:

  • Literature review of studies on ER function and cardiovascular disease.
  • Analysis of molecular mechanisms linking ER stress to atherosclerotic processes.
  • Discussion of preclinical and clinical data relevant to ER stress modulation.

Main Results:

  • Endoplasmic reticulum (ER) dysfunction is implicated in various human diseases, including atherosclerosis.
  • Evidence suggests ER stress contributes to the initiation and advancement of atherosclerotic lesions.
  • Specific molecular pathways within the ER are associated with inflammatory responses in atherosclerosis.

Conclusions:

  • Endoplasmic reticulum (ER) stress is a significant factor in the pathogenesis of atherosclerosis.
  • Modulating ER stress pathways presents a promising avenue for novel anti-atherogenic therapies.
  • Further research into ER stress mechanisms could lead to effective treatments for cardiovascular disease.

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