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Protein & Peptide Letters


ISSN (Print): 0929-8665
ISSN (Online): 1875-5305

Review Article

Renin Angiotensin System and Cytokines in Chronic Kidney Disease: Clinical and Experimental Evidence

Author(s): Ariadna Andrade Saldanha da Silva, Thiago Ruiz Rodrigues Prestes, Amanda Oliveira Lauar, Bernardo Bahia Finotti and Ana Cristina Simoes e Silva*

Volume 24, Issue 9, 2017

Page: [799 - 808] Pages: 10

DOI: 10.2174/0929866524666170818160809

Price: $65


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.

Keywords: Chronic kidney disease, renin-angiotensin system, cytokines, Angiotensin-(1-7), ACE2, Mas receptor.

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