Genetic variants of the renin angiotensin system: Effects on atherosclerosis in experimental models and humans

Alan Daugherty, Aruna Poduri, Xiaofeng Chen, Hong Lu, Lisa A. Cassis

Research output: Contribution to journalReview articlepeer-review

11 Scopus citations

Abstract

The renin angiotensin system (RAS) has profound effects on atherosclerosis development in animal models, which is partially complimented by evidence in the human disease. Although angiotensin II was considered to be the principal effector of the RAS, a broader array of bioactive angiotensin peptides have been identified that have increased the scope of enzymes and receptors in the RAS. Genetic interruption of the synthesis of these peptides has not been extensively performed in experimental or human studies. A few studies demonstrate that interruption of a component of the angiotensin peptide synthesis pathway reduces experimental lesion formation. The evidence in human studies has not been consistent. Conversely, genetic manipulation of the RAS receptors has demonstrated that AT1a receptors are profoundly involved in experimental atherosclerosis. Few studies have reported links of genetic variants of angiotensin II receptors to human atherosclerotic diseases. Further genetic studies are needed to define the role of RAS in atherosclerosis.

Original languageEnglish
Pages (from-to)167-173
Number of pages7
JournalCurrent Atherosclerosis Reports
Volume12
Issue number3
DOIs
StatePublished - May 2010

Bibliographical note

Funding Information:
Acknowledgments The authors’ work in this area is supported by the National Institutes of Health (HL62846). We also acknowledge the editorial assistance of Debra L. Rateri.

Keywords

  • Atherosclerosis
  • Genetic variants
  • Renin angiotensin

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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