Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2015 Feb;179(2):137-45.
doi: 10.1111/cei.12467.

Angiotensin II in inflammation, immunity and rheumatoid arthritis

Affiliations
Review

Angiotensin II in inflammation, immunity and rheumatoid arthritis

Y Chang et al. Clin Exp Immunol. 2015 Feb.

Abstract

Rheumatoid arthritis (RA) is an autoimmune inflammatory disease that is characterized by increased cardiovascular morbidity and mortality, independent of the traditional risk factors for cardiovascular disease. Although classically known for its role in the regulation of circulatory homeostasis, angiotensin II (Ang II) is recognized to act as a powerful proinflammatory mediator. Some research has showed that Ang II plays important roles in autoimmune diseases, including RA, systemic lupus erythematosus and multiple sclerosis. Ang II blockers prove effective in reducing inflammation and autoimmunity in rheumatic diseases and their relative safety, together with their effects for reducing the cardiovascular disease risk, suggest that Ang II blockers may at least act as effective adjunctive therapy for disease control in patients with RA. The present review focuses systematically on the potential impact of Ang II and its receptors on inflammation and immunomodulation in patients with RA.

Keywords: angiotensin II; immunity; inflammation; rheumatoid arthritis.

PubMed Disclaimer

Figures

Figure 1
Figure 1
The roles of angiotensin II (Ang II) on innate and adaptive immunity. Ang II via Ang II type 1A receptor (AT1R) signalling in immune cells contributes to the inflammatory responses and activation of the immune system.
Figure 2
Figure 2
Model of the mechanisms of action of angiotensin II (Ang II) receptor blockers (ARBs). Under Ang II type 1A receptor (AT1R) blockade, the enhancing Ang II levels may result in increased activation of AT2R. In this way, the ability of Ang II to stimulate AT2R in the presence of blockade of AT1R could provide additional complementary therapeutic benefit.

References

    1. Aviña-Zubieta JA, Choi HK, Sadatsafavi M. Risk of cardiovascular mortality in patients with RA: a meta-analysis of observational studies. Arthritis Rheum. 2008;59:1690–1697. - PubMed
    1. Meune C, Touzé E, Trinquart L, Allanore Y. High risk of clinical cardiovascular events in RA: levels of associations of myocardial infarction and stroke through a systematic review and meta-analysis. Arch Cardiovasc Dis. 2010;103:253–261. - PubMed
    1. Dessein PH, Norton GR, Woodiwiss AJ, Joffe BI, Wolfe F. Influence of nonclassical cardiovascular risk factors on the accuracy of predicting subclinical atherosclerosis in RA. J Rheumatol. 2007;34:943–951. - PubMed
    1. Solomon DH, Kremer J, Curtis JR. Explaining the cardiovascular risk associated with RA traditional risk factors versus markers of RA severity. Ann Rheum Dis. 2010;69:1920–1925. - PMC - PubMed
    1. Libby P. Role of inflammation in atherosclerosis associated with rheumatoid arthritis. Am J Med. 2008;121:S21–31. - PubMed

Publication types

MeSH terms