Mechanisms of the Renin Angiotensin System Influencing Atherosclerosis

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

Abstract

This chapter focuses on recent mechanistic studies in animal models. Genetic manipulation and pharmacological approaches strongly enhance the understanding on how the Renin Angiotensin System (RAS) influences atherosclerosis. The chapter updates the current knowledge regarding the roles of cell-specific manipulation of the RAS components on atherosclerosis and molecules that influence atherosclerosis via activation of Angiotensin II (Angll). Using hypercholesterolemic mouse models with chronic AngII infusion (typically 0.5 or 1 μg/kg/min for 4 weeks), many potential molecular mechanisms by which the bioactive angiotensin peptide promotes atherosclerosis are studied. The chapter also provides impressively consistent demonstrations that activation of AngII augments atherosclerosis, while inhibition of renin, Angiotensin converting enzyme (ACE), or AT1 receptor attenuates atherosclerosis in animal models. The feedback loop formed between animal experiments and clinical trials will continuously be a powerful approach to enhance knowledge of the complex disease and provide mechanistic base in improving current therapeutic strategies.

Original languageEnglish
Title of host publicationAtherosclerosis
Subtitle of host publicationRisks, Mechanisms, and Therapies
Pages207-219
Number of pages13
ISBN (Electronic)9781118828533
DOIs
StatePublished - Mar 27 2015

Keywords

  • Angiotensin converting enzyme (ACE)
  • AT1 receptor
  • Atherosclerosis
  • Renin Angiotensin System (RAS)

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology (all)

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