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Renin Angiotensin System and Cytokines in Chronic Kidney Disease: Clinical and Experimental Evidence
Ariadna Andrade Saldanha da Silva1, Thiago Ruiz Rodrigues Prestes1, Amanda Oliveira Lauar1
1Interdisciplinary Laboratory of Medical Investigation, Faculty of Medicine, Federal University of Minas Gerais (UFMG), Brazil.
Introduction:
Chronic kidney disease (CKD) has been considered an important public health issue in all countries. Experimental and clinical studies support the general idea that the pathophysiology of CKD is associated with the interaction of several endogenous mediators, including components of the renin-angiotensin system (RAS) and cytokines.
Objective:
This review aims to report available evidence on the interaction of RAS molecules and cytokines in CKD.
Results:
Therapeutic administration of angiotensin converting enzyme (ACE) inhibitors and/or angiotensin type 1 (AT1) receptor antagonists can slow down the deterioration of renal function. These medications reduce the formation (ACE inhibitor) or the receptor-mediated effects of Angiotensin II (AT1 antagonist) and by so doing inhibit cytokine-mediated kidney tissue inflammation. In sharp contrast, the activation of ACE2, the stimulation of Angiotensin-(1-7) synthesis and/or the effects mediated by its G-protein coupled receptor, named Mas receptor, ameliorates experimental renal injury by reducing renal tissue inflammation and fibrosis in many experimental models of renal diseases.
Conclusion:
Novel compounds that activate and/or stimulate ACE2-Angiontensin-(1-7)-Mas receptor axis may also play a role in the treatment of CKD, mainly by controlling inflammatory response and pathways of fibrosis at kidney tissue. Clinical trials with these new pharmacological compounds will, in due course, determine whether this promise will become a helpful treatment.
Insights
Chronic kidney disease (CKD) involves renin-angiotensin system (RAS) and cytokines. Targeting the ACE2-Angiotensin-(1-7)-Mas receptor axis shows promise for treating kidney inflammation and fibrosis in CKD.
Area of Science:
- Nephrology
- Cardiovascular Research
- Immunology
Background:
- Chronic kidney disease (CKD) is a significant global public health concern.
- CKD pathophysiology involves complex interactions between endogenous mediators, including the renin-angiotensin system (RAS) and cytokines.
Purpose of the Study:
- To review existing evidence on the interplay between RAS molecules and cytokines in the context of CKD.
- To explore potential therapeutic targets within the RAS for managing kidney disease.
Main Methods:
- Literature review of experimental and clinical studies.
- Analysis of the roles of angiotensin-converting enzyme (ACE) inhibitors, AT1 receptor antagonists, and the ACE2-Angiotensin-(1-7)-Mas receptor axis in renal pathophysiology.
Main Results:
- ACE inhibitors and AT1 receptor antagonists slow renal function decline by inhibiting Angiotensin II-mediated inflammation.
- Activation of the ACE2-Angiotensin-(1-7)-Mas receptor pathway demonstrates protective effects, reducing inflammation and fibrosis in experimental kidney disease models.
Conclusions:
- The ACE2-Angiotensin-(1-7)-Mas receptor axis presents a promising therapeutic target for CKD.
- Compounds stimulating this axis may help control kidney inflammation and fibrosis, warranting further clinical investigation.
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