Atherosclerosis: Known and unknown

Jianglin Fan1,2, Teruo Watanabe3

  • 1Department of Molecular Pathology, Faculty of Medicine, Interdisciplinary Graduate School of Medical Sciences, University of Yamanashi, Chuo, Japan.

Pathology International
|January 25, 2022
PubMed

Insights

Atherosclerosis, a leading global killer, involves complex pathology and pathogenesis influenced by genetics and environment. New models and therapies are needed for patients unresponsive to statins.

Area of Science:

  • Cardiovascular Science
  • Pathology
  • Molecular Biology

Background:

  • Atherosclerosis is a major cause of death globally, stemming from genetic and environmental factors.
  • Known risk factors include hypercholesterolemia, hypertension, diabetes, and smoking, contributing to vascular chronic inflammation.
  • While statins are effective, many patients require novel treatments due to incomplete response.

Purpose of the Study:

  • To review the pathology and pathogenesis of atherosclerosis.
  • To discuss current understanding and identify unanswered questions in atherosclerosis research.
  • To highlight the need for new animal models and therapeutic strategies.

Main Methods:

  • Review of existing literature on atherosclerosis pathology and pathogenesis.
  • Analysis of molecular mechanisms investigated through genetically modified animal models.
  • Evaluation of the efficacy of current treatments like statins.

Main Results:

  • Atherosclerosis develops over decades, involving chronic inflammation and interactions between risk factors and arterial cells.
  • Genetically modified animals have advanced understanding of molecular mechanisms.
  • Statins represent the most effective current treatment for prevention and management.

Conclusions:

  • Despite progress, the complete pathogenesis of atherosclerosis remains incompletely understood.
  • There is a critical need for innovative therapeutic approaches for statin-resistant patients.
  • Development of new animal models is essential for further research into atherosclerosis.

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