Cellular and molecular mechanisms of atherosclerosis with mouse models

Ryuji Ohashi1, Hong Mu, Qizhi Yao

  • 1Molecular Surgeon Research Center, Division of Vascular Surgery and Endovascular Therapy, Michael E. DeBakey Department of Surgery, Baylor College of Medicine and The Methodist Hospital, Houston 77030, Texas, USA.

Insights

Genetically engineered mouse models, including LDLR(-/-) and apoE(-/-) mice, have revolutionized atherosclerosis research. Modified models now better mimic human disease, advancing our understanding of cardiovascular disease.

Area of Science:

  • * Cardiovascular Research
  • * Genetically Engineered Mouse Models

Background:

  • * Atherosclerosis research has significantly advanced through the use of genetically engineered mouse models.
  • * Traditional models like low-density lipoprotein receptor knockout (LDLR(-/-)) and apolipoprotein E knockout (apoE(-/-)) mice have been foundational.
  • * Recent developments focus on modified models that more accurately replicate human atherosclerotic lesions.

Purpose of the Study:

  • * To review various types of mouse models used in atherosclerosis research.
  • * To highlight the contributions of these models to current research advancements.
  • * To discuss modifications enhancing disease characterization.

Main Methods:

  • * Review of existing literature on genetically engineered mouse models for atherosclerosis.
  • * Analysis of modifications applied to traditional mouse models.
  • * Focus on models incorporating inflammation, hypertension, and immune system variations.

Main Results:

  • * Genetically engineered mouse models have dramatically accelerated atherosclerosis research.
  • * Modified models now incorporate key human disease characteristics like inflammation and altered glucose metabolism.
  • * These advanced models provide deeper insights into disease mechanisms.

Conclusions:

  • * Mouse models are indispensable tools in atherosclerosis research.
  • * Ongoing modifications continue to improve their translational relevance to human cardiovascular disease.
  • * The evolution of these models drives progress in understanding and treating atherosclerosis.