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Angiotensin II as a pro-inflammatory mediator
M Ian Phillips1, Shuntaro Kagiyama
1Department of Physiology, College of Medicine, University of Florida, Gainesville 32610, USA. MIP@ufl.edu
Current Opinion in Investigational Drugs (London, England : 2000)
|July 2, 2002
Summary
Angiotensin II (Ang II) drives atherosclerosis by promoting inflammation and plaque instability. Inhibiting Ang II pathways, like with ACE inhibitors, may treat this cardiovascular disease.
Area of Science:
- Cardiovascular Science
- Inflammation Biology
- Renal Physiology
Background:
- The renin-angiotensin system (RAS) component, Angiotensin II (Ang II), is linked to hypertension and renal failure.
- Ang II promotes inflammation, contributing to atherosclerotic plaque development and rupture.
- Key RAS components, Angiotensin Converting Enzyme (ACE) and Angiotensin II type 1 receptors (AT1), are elevated in atherosclerotic lesions.
Purpose of the Study:
- To elucidate the role of Angiotensin II (Ang II) in the pathogenesis of atherosclerosis.
- To investigate the molecular mechanisms by which Ang II influences inflammatory processes in atherosclerotic plaques.
- To assess the potential therapeutic implications of targeting the RAS in atherosclerosis treatment.
Main Methods:
- Review of existing literature on Ang II, RAS, and atherosclerosis.
- Analysis of the role of Ang II in stimulating inflammatory pathways, including NFkappaB activation.
- Examination of the expression levels of AT1 and ACE in atherosclerotic plaques.
Main Results:
- Ang II significantly contributes to atherosclerotic plaque formation and instability through pro-inflammatory actions.
- Ang II upregulates nuclear factor-kappaB (NFkappaB), leading to increased expression of inflammatory cytokines like IL-6 and MCP-1.
- Elevated levels of AT1 receptors and ACE are observed in atherosclerotic plaques, particularly within monocytes.
Conclusions:
- Angiotensin II is a critical factor in the development, inflammation, and stability of atherosclerotic plaques.
- Targeting Ang II signaling pathways, via AT1 receptor antagonists or ACE inhibitors, represents a promising therapeutic strategy for atherosclerosis.