Renin Angiotensin System and Cytokines in Chronic Kidney Disease: Clinical and Experimental Evidence
| Autor: | Amanda Oliveira Lauar, Ariádna Andrade Saldanha da Silva, Bernardo Bahia Finotti, Thiago Ruiz Rodrigues Prestes, Ana Cristina Simões e Silva |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Angiotensins Angiotensin-Converting Enzyme Inhibitors Blood Pressure Pharmacology Kidney Biochemistry Receptors G-Protein-Coupled Renin-Angiotensin System 03 medical and health sciences Structural Biology Fibrosis Internal medicine Renin–angiotensin system Animals Humans Medicine Renal Insufficiency Chronic Angiotensin II receptor type 1 biology business.industry Angiotensin-converting enzyme General Medicine medicine.disease Angiotensin II 030104 developmental biology Endocrinology medicine.anatomical_structure ACE inhibitor biology.protein Cytokines business Angiotensin II Type 1 Receptor Blockers medicine.drug Kidney disease |
| Zdroj: | Protein & Peptide Letters. 24 |
| ISSN: | 0929-8665 |
| DOI: | 10.2174/0929866524666170818160809 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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