The role of the renin–angiotensin system in thoracic aortic aneurysms: Clinical implications

2011 ◽  
Vol 131 (1) ◽  
pp. 50-60 ◽  
Author(s):  
Els Moltzer ◽  
Jeroen Essers ◽  
Joep H.M. van Esch ◽  
Jolien W. Roos-Hesselink ◽  
A.H. Jan Danser
Keyword(s):  
Renin Angiotensin System ◽  
Aortic Aneurysms ◽  
Clinical Implications ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Thoracic Aortic Aneurysms

Involvement of the renin–angiotensin system in abdominal and thoracic aortic aneurysms

2012 ◽  
Vol 123 (9) ◽  
pp. 531-543 ◽  
Author(s):  
Hong Lu ◽  
Debra L. Rateri ◽  
Dennis Bruemmer ◽  
Lisa A. Cassis ◽  
Alan Daugherty
Keyword(s):  
Animal Models ◽  
Aortic Rupture ◽  
Association Studies ◽  
Renin Angiotensin System ◽  
Pharmacological Therapy ◽  
Aortic Aneurysms ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Thoracic Aortic Aneurysms

Aortic aneurysms are relatively common maladies that may lead to the devastating consequence of aortic rupture. AAAs (abdominal aortic aneurysms) and TAAs (thoracic aortic aneurysms) are two common forms of aneurysmal diseases in humans that appear to have distinct pathologies and mechanisms. Despite this divergence, there are numerous and consistent demonstrations that overactivation of the RAS (renin–angiotensin system) promotes both AAAs and TAAs in animal models. For example, in mice, both AAAs and TAAs are formed during infusion of AngII (angiotensin II), the major bioactive peptide in the RAS. There are many proposed mechanisms by which the RAS initiates and perpetuates aortic aneurysms, including effects of AngII on a diverse array of cell types and mediators. These experimental findings are complemented in humans by genetic association studies and retrospective analyses of clinical data that generally support a role of the RAS in both AAAs and TAAs. Given the lack of a validated pharmacological therapy for any form of aortic aneurysm, there is a pressing need to determine whether the consistent findings on the role of the RAS in animal models are translatable to humans afflicted with these diseases. The present review compiles the recent literature that has shown the RAS as a critical component in the pathogenesis of aortic aneurysms.

scholarly journals Role of the renin-angiotensin system on abdominal aortic aneurysms

2013 ◽  
Vol 43 (12) ◽  
pp. 1328-1338 ◽  
Author(s):  
Sonaz Malekzadeh ◽  
Rodrigo A. Fraga-Silva ◽  
Bram Trachet ◽  
Fabrizio Montecucco ◽  
François Mach ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
Abdominal Aortic Aneurysms ◽  
Aortic Aneurysms ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Abdominal Aortic

scholarly journals Transforming Growth Factor-β and the Renin-Angiotensin System in Syndromic Thoracic Aortic Aneurysms: Implications for Treatment

2020 ◽  
Author(s):  
Daan C.H. van Dorst ◽  
Nathalie P. de Wagenaar ◽  
Ingrid van der Pluijm ◽  
Jolien W. Roos-Hesselink ◽  
Jeroen Essers ◽  
...  
Keyword(s):  
Growth Factor ◽  
Medical Treatment ◽  
Transforming Growth Factor ◽  
Renin Angiotensin System ◽  
Transforming Growth Factor Β ◽  
Aortic Aneurysms ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Thoracic Aortic Aneurysms ◽  
Β Blockers

AbstractThoracic aortic aneurysms (TAAs) are permanent pathological dilatations of the thoracic aorta, which can lead to life-threatening complications, such as aortic dissection and rupture. TAAs frequently occur in a syndromic form in individuals with an underlying genetic predisposition, such as Marfan syndrome (MFS) and Loeys-Dietz syndrome (LDS). Increasing evidence supports an important role for transforming growth factor-β (TGF-β) and the renin-angiotensin system (RAS) in TAA pathology. Eventually, most patients with syndromic TAAs require surgical intervention, as the ability of present medical treatment to attenuate aneurysm growth is limited. Therefore, more effective medical treatment options are urgently needed. Numerous clinical trials investigated the therapeutic potential of angiotensin receptor blockers (ARBs) and β-blockers in patients suffering from syndromic TAAs. This review highlights the contribution of TGF-β signaling, RAS, and impaired mechanosensing abilities of aortic VSMCs in TAA formation. Furthermore, it critically discusses the most recent clinical evidence regarding the possible therapeutic benefit of ARBs and β-blockers in syndromic TAA patients and provides future research perspectives and therapeutic implications.

Role of genetic variability in the renin-angiotensin system in diabetic and nondiabetic renal disease

2001 ◽  
Vol 21 (6) ◽  
pp. 580-592 ◽  
Author(s):  
Arnold Boonstra ◽  
Dick de Zeeuw ◽  
Paul E. de Jong ◽  
Gerjan Navis
Keyword(s):  
Genetic Variability ◽  
Renal Disease ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

The Renin Angiotensin System and Bipolar Disorder: A Systematic Review

2020 ◽  
Vol 27 (6) ◽  
pp. 520-528 ◽  
Author(s):  
Izabela Guimarães Barbosa ◽  
Giulia Campos Ferreira ◽  
Diomildo Ferreira Andrade Júnior ◽  
Cássio Rocha Januário ◽  
André Rolim Belisário ◽  
...  
Keyword(s):  
Systematic Review ◽  
Bipolar Disorder ◽  
Cardiovascular Diseases ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin Receptors ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Search Terms

Bipolar Disorder (BD) is a chronic a multifactorial psychiatric illness that affects mood, cognition, and functioning. BD is associated with several psychiatric conditions as well clinical comorbidities, particularly cardiovascular diseases. The neurobiology of BD is complex and multifactorial and several systems have been implicated. Considering that the Renin Angiotensin System (RAS) plays an important role in cardiovascular diseases and that recently evidence has suggested its role in psychiatric disorders, the aim of the present study is to summarize and to discuss recent findings related to the modulation of RAS components in BD. A systematic search of the literature using the electronic databases MEDLINE and LILACS was conducted through March 2019. The search terms were: “Bipolar Disorder”; “Renin Angiotensin System”; “Angiotensin 2”; “Angiotensin receptors”; “Angiotensin 1-7”; “ACE”; “ACE2”; “Mas Receptor”. We included original studies assessing RAS in BD patients. Two hundred twenty-two citations were initially retrieved. Eleven studies were included in our systematic review. In the majority of studies (6 of 8), the ACE insertion/deletion (I/D) polymorphism did not differ between BD patients and controls. BD patients presented higher plasma renin activity in comparison with controls. The studies evaluating the RAS molecules in BD are very scarce and heterogeneous. The literature suggests a potential role of RAS in BD. Further studies are necessary to investigate this relationship.

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