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Published on: June 7, 2016
The renin-angiotensin system and atherosclerosis
1Service of Vascular Medicien, Department of Internal Medicine, CHUV (Hôpital Nestlé), Av. Pierre Decker 5, 1011 Lausanne, Switzerland. lucia.mazzolai@chuv.ch
Insights
The renin-angiotensin system and its peptide angiotensin II may drive atherosclerosis progression and plaque vulnerability. Understanding these mechanisms is crucial for managing this complex arterial disease.
Area of Science:
- Cardiovascular Science
- Vascular Biology
- Medical Research
Background:
- Atherosclerosis is a complex arterial disease involving lipid deposition, inflammation, and fibrous elements.
- Vulnerable plaques, a progression of early fatty streaks, pose significant clinical risks.
- Mechanisms driving plaque instability from a stable state remain largely unknown.
Purpose of the Study:
- To investigate the role of the renin-angiotensin system (RAS) and angiotensin II in atherosclerosis development.
- To explore the potential contribution of angiotensin II to plaque vulnerability and progression.
- To elucidate the direct effects of angiotensin II beyond blood pressure regulation in atherosclerosis.
Main Methods:
- Review of epidemiologic, experimental, and clinical studies on RAS and atherosclerosis.
- Analysis of recent research on angiotensin II's role in plaque instability.
- Examination of direct cellular and molecular mechanisms involved.
Main Results:
- Epidemiologic, experimental, and clinical data support the RAS's contribution to atherosclerosis.
- Angiotensin II, the active peptide of RAS, influences atherosclerosis development and progression.
- Emerging evidence suggests angiotensin II acts as a mediator of plaque vulnerability.
Conclusions:
- The renin-angiotensin system, particularly angiotensin II, plays a multifaceted role in atherosclerosis.
- Angiotensin II contributes directly to disease progression and plaque vulnerability.
- Further research into RAS modulation may offer therapeutic strategies for atherosclerosis.
Abstract:
Atherosclerosis is an insidious and complex disease of large- and medium-sized arteries. The primum movens of the disease is characterized by co-localization of lipids, inflammatory cells, and fibrous elements within the intima of vessels. Starting as a "fatty streak," the disease evolves over decades into complex lesions that can progress toward a stable or a vulnerable plaque. During the past decade, we have become familiar with the features of the vulnerable plaque; however, the mechanisms that cause a stable plaque to change into a vulnerable lesion with its dramatic clinical outcome still remain largely unknown. There is good evidence from epidemiologic, experimental, and clinical studies that the renin-angiotensin system, via its active peptide angiotensin II, may contribute to atherosclerosis development and progression, not only by increasing blood pressure but also through multiple direct effects. Moreover, recent studies have shown a potential role for angiotensin II as a mediator of plaque vulnerability.
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