The Renin-Angiotensin-Aldosterone System in Vascular Inflammation and Remodeling

The RAAS through its physiological effectors plays a key role in promoting and maintaining inflammation. Inflammation is an important mechanism in the development and progression of CVD such as hypertension and atherosclerosis. In addition to its main role in regulating blood pressure and its role i...

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Main Authors: Maricica Pacurari, Ramzi Kafoury, Paul B. Tchounwou, Kenneth Ndebele
Format: Article
Language:English
Published: Wiley 2014-01-01
Series:International Journal of Inflammation
Online Access:http://dx.doi.org/10.1155/2014/689360
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author Maricica Pacurari
Ramzi Kafoury
Paul B. Tchounwou
Kenneth Ndebele
author_facet Maricica Pacurari
Ramzi Kafoury
Paul B. Tchounwou
Kenneth Ndebele
author_sort Maricica Pacurari
collection DOAJ
description The RAAS through its physiological effectors plays a key role in promoting and maintaining inflammation. Inflammation is an important mechanism in the development and progression of CVD such as hypertension and atherosclerosis. In addition to its main role in regulating blood pressure and its role in hypertension, RAAS has proinflammatory and profibrotic effects at cellular and molecular levels. Blocking RAAS provides beneficial effects for the treatment of cardiovascular and renal diseases. Evidence shows that inhibition of RAAS positively influences vascular remodeling thus improving CVD outcomes. The beneficial vascular effects of RAAS inhibition are likely due to decreasing vascular inflammation, oxidative stress, endothelial dysfunction, and positive effects on regeneration of endothelial progenitor cells. Inflammatory factors such as ICAM-1, VCAM-1, TNFα, IL-6, and CRP have key roles in mediating vascular inflammation and blocking RAAS negatively modulates the levels of these inflammatory molecules. Some of these inflammatory markers are clinically associated with CVD events. More studies are required to establish long-term effects of RAAS inhibition on vascular inflammation, vascular cells regeneration, and CVD clinical outcomes. This review presents important information on RAAS’s role on vascular inflammation, vascular cells responses to RAAS, and inhibition of RAAS signaling in the context of vascular inflammation, vascular remodeling, and vascular inflammation-associated CVD. Nevertheless, the review also equates the need to rethink and rediscover new RAAS inhibitors.
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spelling doaj-art-24bf89d98ec6479c897243b83e81bd9c2025-02-03T01:23:28ZengWileyInternational Journal of Inflammation2090-80402042-00992014-01-01201410.1155/2014/689360689360The Renin-Angiotensin-Aldosterone System in Vascular Inflammation and RemodelingMaricica Pacurari0Ramzi Kafoury1Paul B. Tchounwou2Kenneth Ndebele3Biology Department, College of Engineering, Science, and Technology, Jackson State University, Jackson, MS 39217, USABiology Department, College of Engineering, Science, and Technology, Jackson State University, Jackson, MS 39217, USABiology Department, College of Engineering, Science, and Technology, Jackson State University, Jackson, MS 39217, USABiology Department, College of Engineering, Science, and Technology, Jackson State University, Jackson, MS 39217, USAThe RAAS through its physiological effectors plays a key role in promoting and maintaining inflammation. Inflammation is an important mechanism in the development and progression of CVD such as hypertension and atherosclerosis. In addition to its main role in regulating blood pressure and its role in hypertension, RAAS has proinflammatory and profibrotic effects at cellular and molecular levels. Blocking RAAS provides beneficial effects for the treatment of cardiovascular and renal diseases. Evidence shows that inhibition of RAAS positively influences vascular remodeling thus improving CVD outcomes. The beneficial vascular effects of RAAS inhibition are likely due to decreasing vascular inflammation, oxidative stress, endothelial dysfunction, and positive effects on regeneration of endothelial progenitor cells. Inflammatory factors such as ICAM-1, VCAM-1, TNFα, IL-6, and CRP have key roles in mediating vascular inflammation and blocking RAAS negatively modulates the levels of these inflammatory molecules. Some of these inflammatory markers are clinically associated with CVD events. More studies are required to establish long-term effects of RAAS inhibition on vascular inflammation, vascular cells regeneration, and CVD clinical outcomes. This review presents important information on RAAS’s role on vascular inflammation, vascular cells responses to RAAS, and inhibition of RAAS signaling in the context of vascular inflammation, vascular remodeling, and vascular inflammation-associated CVD. Nevertheless, the review also equates the need to rethink and rediscover new RAAS inhibitors.http://dx.doi.org/10.1155/2014/689360
spellingShingle Maricica Pacurari
Ramzi Kafoury
Paul B. Tchounwou
Kenneth Ndebele
The Renin-Angiotensin-Aldosterone System in Vascular Inflammation and Remodeling
International Journal of Inflammation
title The Renin-Angiotensin-Aldosterone System in Vascular Inflammation and Remodeling
title_full The Renin-Angiotensin-Aldosterone System in Vascular Inflammation and Remodeling
title_fullStr The Renin-Angiotensin-Aldosterone System in Vascular Inflammation and Remodeling
title_full_unstemmed The Renin-Angiotensin-Aldosterone System in Vascular Inflammation and Remodeling
title_short The Renin-Angiotensin-Aldosterone System in Vascular Inflammation and Remodeling
title_sort renin angiotensin aldosterone system in vascular inflammation and remodeling
url http://dx.doi.org/10.1155/2014/689360
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