Control of atherosclerotic plaque vulnerability: insights from transgenic mice

Sylvia Heeneman1, Esther Lutgens, Kitty B Schapira

  • 1Department of Pathology, Maastricht University, Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands. s.heeneman@path.unimaas.nl

Insights

Genetically-engineered mouse models are crucial for understanding atherosclerosis progression and plaque vulnerability. These models help researchers investigate molecular mechanisms and develop strategies to control vulnerable atherosclerotic plaques.

Area of Science:

  • Cardiovascular Biology
  • Translational Medicine
  • Genetics

Background:

  • Atherosclerosis is a complex, progressive arterial disease involving lipid and cellular accumulation.
  • Understanding the molecular mechanisms of atherosclerotic plaque progression is critical.
  • Genetically-engineered mouse models offer valuable tools for studying this disease.

Purpose of the Study:

  • To review the relevance, advantages, and disadvantages of genetically-engineered mice for investigating plaque vulnerability mechanisms.
  • To highlight insights gained from these models for controlling plaque vulnerability.

Main Methods:

  • Review of existing literature on genetically-engineered mouse models in atherosclerosis research.
  • Analysis of how genetic manipulations in mice affect key aspects of plaque development and vulnerability.
  • Comparison of features in mouse lesions to human vulnerable plaques.

Main Results:

  • Genetically-engineered mice replicate key features of human vulnerable atherosclerotic lesions.
  • Manipulations in apoptosis, lipid metabolism, inflammation, matrix remodeling, and thrombosis pathways are effectively studied in mice.
  • These models provide insights into the control of plaque vulnerability.

Conclusions:

  • Genetically-engineered mouse models are indispensable for dissecting the molecular underpinnings of atherosclerosis and plaque vulnerability.
  • These models facilitate the identification of therapeutic targets for managing vulnerable atherosclerotic plaques.
  • Further utilization of these models will advance strategies for controlling atherosclerosis progression.

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