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A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
Published on: October 26, 2020
Anti-inflammatory properties of drugs acting on the renin-angiotensin system
Luigi Sironi1, Elena Nobili, Anita Gianella
1Department of Pharmacological Sciences, University of Milan, Italy. luigi.sironi@unimi.it
Abstract:
It is now well established that the activation of the renin-angiotensin system (RAS) is involved in the onset and progression of cardiovascular and renal diseases, and that its main effector, angiotensin II (Ang II) has major pro-inflammatory activity that induces the expression of cytokines, chemokines, adhesion molecules, growth factors and reactive oxygen species. By means of these actions, Ang II induces vascular inflammation, endothelial dysfunction and fibrosis, and participates in destabilizing atherosclerotic plaque and establishing chronic kidney diseases. Blocking the RAS by inhibiting Ang II generation or blocking angiotensin receptors reduces the morbidity and mortality associated with cardiovascular and renal disease beyond the levels due to the lowering of blood pressure, and these benefits are at least partially due to the reduction/prevention of both local and systemic inflammatory processes. The aim of this review is to describe the role of the RAS (and particularly Ang II) in initiating and maintaining these processes, and to summarize experimental and clinical evidence supporting the role of drugs acting on the RAS in preventing or modulating inflammation.
Insights
The renin-angiotensin system (RAS) and its effector angiotensin II (Ang II) drive inflammation in cardiovascular and kidney diseases. Blocking the RAS reduces disease progression and inflammation, offering benefits beyond blood pressure reduction.
Area of Science:
- Cardiovascular Science
- Renal Science
- Inflammation Biology
Background:
- The renin-angiotensin system (RAS) is implicated in cardiovascular and renal diseases.
- Angiotensin II (Ang II), the main RAS effector, promotes inflammation via cytokines, chemokines, and reactive oxygen species.
- Ang II contributes to vascular inflammation, endothelial dysfunction, fibrosis, atherosclerosis, and chronic kidney disease.
Purpose of the Study:
- To review the role of the RAS, particularly Ang II, in initiating and maintaining inflammatory processes.
- To summarize evidence for RAS-targeting drugs in preventing or modulating inflammation.
Main Methods:
- Literature review of experimental and clinical studies.
- Analysis of the mechanisms by which Ang II induces inflammation.
- Evaluation of the impact of RAS blockade on inflammatory processes.
Main Results:
- RAS activation and Ang II are key drivers of inflammation in cardiovascular and renal pathologies.
- Ang II mediates vascular inflammation, endothelial dysfunction, fibrosis, and atherosclerotic plaque destabilization.
- RAS blockade significantly reduces cardiovascular and renal morbidity and mortality, partly by mitigating inflammation.
Conclusions:
- The RAS plays a critical role in initiating and perpetuating inflammation in cardiovascular and renal diseases.
- Drugs targeting the RAS demonstrate efficacy in preventing or modulating these inflammatory processes.
- RAS inhibition offers therapeutic benefits beyond blood pressure control by reducing inflammation.
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