scholarly journals The Role of the Renin-Angiotensin-Aldosterone System in Cardiovascular Disease: Pathogenetic Insights and Clinical Implications

2021 ◽  
Author(s):  
Violeta Capric ◽  
Harshith Priyan Chandrakumar ◽  
Jessica Celenza-Salvatore ◽  
Amgad N. Makaryus
Keyword(s):  
Cardiovascular Disease ◽  
Renal Disease ◽  
Clinical Implications ◽  
Pathological Changes ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Raas Blockade ◽  
Adverse Remodeling ◽  
Artery Disease

Increased attention has been placed on the activation of the renin-angiotensin-aldosterone system (RAAS) and pathogenetic mechanisms in cardiovascular disease. Multiple studies have presented data to suggest that cardiac and arterial stiffness leading to adverse remodeling of both the heart and vasculature leads to the various pathological changes seen in coronary artery disease, heart failure (with preserved and reduced ejection fractions), hypertension and renal disease. Over-activation of the RAAS is felt to contribute to these structural and endocrinological changes through its control of the Na+/K+ balance, fluid volume, and hemodynamic stability. Subsequently, along these lines, multiple large investigations have shown that RAAS blockade contributes to prevention of both cardiovascular and renal disease. We aim to highlight the known role of the activated RAAS and provide an updated description of the mechanisms by which activation of RAAS promotes and leads to the pathogenesis of cardiovascular disease.

Role of the Renin-Angiotensin-Aldosterone System in the Regulation of Plasma Potassium in Chronic Renal Disease

Nephron ◽  
1975 ◽  
Vol 15 (1) ◽  
pp. 35-49 ◽  
Author(s):  
P. Weidmann ◽  
M.H. Maxwell ◽  
P. Rowe ◽  
R. Winer ◽  
S.G. Massry
Keyword(s):  
Renal Disease ◽  
Chronic Renal Disease ◽  
Plasma Potassium ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin

scholarly journals Role of the Renin-Angiotensin-Aldosterone System in Dystrophin-Deficient Cardiomyopathy

2020 ◽  
Author(s):  
Moises Rodriguez-Gonzalez ◽  
Manuel Lubian-Gutierrez ◽  
Helena Maria Cascales-Poyatos ◽  
Alvaro Antonio Perez-Reviriego ◽  
Ana Castellano-Martinez
Keyword(s):  
Therapeutic Strategy ◽  
Clinical Evidence ◽  
Enzyme Inhibitors ◽  
English Literature ◽  
Current Evidence ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Raas Blockade ◽  
Comprehensive Search

Dystrophin-deficient cardiomyopathy (DDC) is currently the leading cause of death in patients with dystrophinopathies. Targeting myocardial fibrosis (MF) has become a major therapeutic goal in order to prevent the occurrence of DDC. We aimed to review and summarize the current evidence about the role of the renin-angiotensin-aldosterone system (RAAS) in the development and perpetuation of MF in DCC. We conducted a comprehensive search of peer-reviewed English literature on PubMed about this subject. We found increasing preclinical evidence from studies in animal models during the last 20 years pointing out a central role of RAAS in the development of MF in DDC. Local tissue RAAS acts directly mainly through its main fibrotic component angiotensin II (ANG2) and its transducer receptor (AT1R) and downstream TGF-b pathway. Also, it modulates the actions of most of the remaining pro-fibrotic factors involved in DDC. Despite limited clinical evidence, RAAS blockade constitutes the most studied, available and promising therapeutic strategy against MF and DDC. Conclusion: Based on the evidence reviewed, it would be recommendable to start RAAS blockade therapy through angiotensin converter enzyme inhibitors (ACEI) or AT1R blockers (ARBs) alone or in combination with mineralocorticoid receptor antagonists (MRa) at the youngest age after the diagnosis of dystrophinopathies, in order to delay the occurrence or slow the progression of MF, even before the detection of any cardiovascular alteration.

scholarly journals Role of MicroRNAs in Renin-Angiotensin-Aldosterone System-Mediated Cardiovascular Inflammation and Remodeling

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Maricica Pacurari ◽  
Paul B. Tchounwou
Keyword(s):  
Gene Expression ◽  
Cardiovascular Disease ◽  
Early Stage ◽  
Inflammatory Factors ◽  
Therapeutic Approaches ◽  
Exact Role ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Endogenous Regulators

MicroRNAs are endogenous regulators of gene expression either by inhibiting translation or protein degradation. Recent studies indicate that microRNAs play a role in cardiovascular disease and renin-angiotensin-aldosterone system- (RAAS-) mediated cardiovascular inflammation, either as mediators or being targeted by RAAS pharmacological inhibitors. The exact role(s) of microRNAs in RAAS-mediated cardiovascular inflammation and remodeling is/are still in early stage of investigation. However, few microRNAs have been shown to play a role in RAAS signaling, particularly miR-155, miR-146a/b, miR-132/122, and miR-483-3p. Identification of specific microRNAs and their targets and elucidating microRNA-regulated mechanisms associated RAS-mediated cardiovascular inflammation and remodeling might lead to the development of novel pharmacological strategies to target RAAS-mediated vascular pathologies. This paper reviews microRNAs role in inflammatory factors mediating cardiovascular inflammation and RAAS genes and the effect of RAAS pharmacological inhibition on microRNAs and the resolution of RAAS-mediated cardiovascular inflammation and remodeling. Also, this paper discusses the advances on microRNAs-based therapeutic approaches that may be important in targeting RAAS signaling.

scholarly journals From preeclampsia to renal disease: a role of angiogenic factors and the renin-angiotensin aldosterone system?

2012 ◽  
Vol 27 (suppl 3) ◽  
pp. iii51-iii57 ◽  
Author(s):  
A. M. van der Graaf ◽  
T. J. Toering ◽  
M. M. Faas ◽  
A. Titia Lely
Keyword(s):  
Renal Disease ◽  
Angiogenic Factors ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin

scholarly journals Role of the Renin–Angiotensin–Aldosterone System in Dystrophin-Deficient Cardiomyopathy

2020 ◽  
Vol 22 (1) ◽  
pp. 356
Author(s):  
Moises Rodriguez-Gonzalez ◽  
Manuel Lubian-Gutierrez ◽  
Helena Maria Cascales-Poyatos ◽  
Alvaro Antonio Perez-Reviriego ◽  
Ana Castellano-Martinez
Keyword(s):  
Therapeutic Strategy ◽  
Clinical Evidence ◽  
Enzyme Inhibitors ◽  
English Literature ◽  
Current Evidence ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Raas Blockade ◽  
Comprehensive Search

Dystrophin-deficient cardiomyopathy (DDC) is currently the leading cause of death in patients with dystrophinopathies. Targeting myocardial fibrosis (MF) has become a major therapeutic goal in order to prevent the occurrence of DDC. We aimed to review and summarize the current evidence about the role of the renin–angiotensin–aldosterone system (RAAS) in the development and perpetuation of MF in DCC. We conducted a comprehensive search of peer-reviewed English literature on PubMed about this subject. We found increasing preclinical evidence from studies in animal models during the last 20 years pointing out a central role of RAAS in the development of MF in DDC. Local tissue RAAS acts directly mainly through its main fibrotic component angiotensin II (ANG2) and its transducer receptor (AT1R) and downstream TGF-b pathway. Additionally, it modulates the actions of most of the remaining pro-fibrotic factors involved in DDC. Despite limited clinical evidence, RAAS blockade constitutes the most studied, available and promising therapeutic strategy against MF and DDC. Conclusion: Based on the evidence reviewed, it would be recommendable to start RAAS blockade therapy through angiotensin converter enzyme inhibitors (ACEI) or AT1R blockers (ARBs) alone or in combination with mineralocorticoid receptor antagonists (MRa) at the youngest age after the diagnosis of dystrophinopathies, in order to delay the occurrence or slow the progression of MF, even before the detection of any cardiovascular alteration.

Abstract 01: The Role of Renin-Angiotensin-Aldosterone System Genes in the Progression of Chronic Kidney Disease: Findings from the Chronic Renal Insufficiency Cohort (CRIC) Study

Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Tanika N Kelly ◽  
Dominic Raj ◽  
Mahboob Rahman ◽  
Matthias Kretzler ◽  
Radhakrishna R Kallem ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Insufficiency ◽  
Renal Disease ◽  
Chronic Renal Insufficiency ◽  
Ckd Progression ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Single Marker

Background: We conducted single-marker, gene-based and pathway-based analyses to examine the association between renin-angiotensin-aldosterone system (RAAS) variants and chronic kidney disease (CKD) progression among Chronic Renal Insufficiency Cohort (CRIC) study participants. Methods: A total of 1,523 white and 1,490 black subjects were genotyped for 490 SNPs in 12 RAAS genes as part of the ITMAT-Broad-CARe array. CKD progression phenotypes included decline in estimated glomerular filtration rate (eGFR) over time and the occurrence of a renal disease event, defined as incident end stage renal disease or halving of eGFR from baseline. Mixed-effects models were used to examine SNP associations with eGFR decline, while Cox proportional hazards models tested SNP associations with renal events. Gene and pathway-based analyses were conducted using the truncated product method. All analyses were stratified by race, and a Bonferroni correction was applied to adjust for multiple testing. Results: Among white and black participants, eGFR declined an average of 1.2 and 2.3 ml/min/1.73m 2 per year, respectively, while renal events occurred in a respective 11.5% and 24.9% of participants. We identified strong gene and pathway-based associations with CKD progression. The AGT and RENBP genes were consistently associated with risk of renal events in separate analyses of white and black participants (all P <1.00х10 -6 ). Driven by the significant gene-based findings, the entire RAAS pathway was also associated with renal events in both groups (both P <1.00х10 -6 ). No single-marker associations with CKD progression were observed. Conclusions: The current study provides strong evidence for a role of the RAAS in CKD progression.

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