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Updated: Aug 14, 2026

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
09:06

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice

Published on: February 20, 2019

Pharmacological basis of different targets for the treatment of atherosclerosis

Harjot K Saini1, Yan-Jun Xu, Amarjit S Arneja

  • 1Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.

Journal of Cellular and Molecular Medicine
|December 21, 2005
PubMed

Insights

Atherosclerosis involves complex cellular changes. New combination therapies targeting inflammation and cell proliferation are needed to improve treatment beyond statins for cardiovascular events.

Area of Science:

  • Cardiovascular Biology
  • Pharmacology
  • Pathophysiology

Background:

  • Atherosclerotic plaque development involves endothelial cells, smooth muscle cells (SMCs), monocytes/macrophages, T-lymphocytes, and platelets.
  • Plaque formation or rupture can lead to acute ischemic events, such as myocardial infarction.
  • Statins are a primary therapy for atherosclerosis by lowering lipids, but their additional benefits suggest new drug targets are needed.

Purpose of the Study:

  • To explore novel therapeutic targets for atherosclerosis beyond lipid reduction.
  • To identify drug strategies that directly impact the atherosclerotic process.
  • To address the challenge of developing combination therapies for improved atherosclerosis management.

Main Methods:

  • Review of current therapeutic strategies and their limitations.
  • Identification of key molecular and cellular pathways involved in atherosclerosis.
  • Analysis of potential targets for pharmacological intervention.

Main Results:

  • Several targets for drug treatment have been recognized, including renin-angiotensin system blockade, nitric oxide augmentation, and calcium influx reduction.
  • Prevention of oxidative stress, inflammation, platelet activation, and SMC proliferation are identified as crucial therapeutic goals.
  • Current therapies like statins offer benefits beyond lipid lowering, highlighting the complexity of the disease.

Conclusions:

  • Developing new drugs that directly target the atherosclerotic process is essential.
  • Combination therapies targeting multiple pathways (inflammation, cell proliferation, etc.) hold promise for improved atherosclerosis treatment.
  • Future research should focus on formulating effective combination therapies to manage atherosclerosis and prevent ischemic events.

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