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Antifibrotic Roles of RAAS Blockers: Update

Authors
  • Zhang, Ying-Ying1
  • Yu, Ying1
  • Yu, Chen1
  • 1 Tongji University School of Medicine,
Type
Published Article
Journal
Renal Fibrosis: Mechanisms and Therapies
Publication Date
Jun 19, 2019
Volume
1165
Pages
671–691
Identifiers
DOI: 10.1007/978-981-13-8871-2_33
PMID: 31399990
PMCID: PMC7121580
Source
PubMed Central
Keywords
License
Unknown

Abstract

The rennin–angiotensin–aldosterone system (RAAS) has been well documented in regulating blood pressure, fluid volume, and sodium balance. Overactivity of RAAS promotes both systemic and regional glomerular capillary hypertension, which could induce hemodynamic injury to the glomerulus, leading to kidney damage and renal fibrosis via profibrotic and proinflammatory pathway. Therefore, the use of RAAS inhibitors (i.e., ACEIs, ARBs, and MRAs) as the optional therapy has been demonstrated to prevent proteinuria, and kidney fibrosis and slow the decline of renal function effectively in the process of kidney disease during the last few decades. Recently, several new components of the RAAS have been discovered, including ACE2 and the corresponding ACE2/Ang (1-7)/Mas axis, which are also present in the kidney. Besides the classic RAAS inhibitors target the angiotensin-AT1-aldosterone axis, with the expanding knowledge about RAAS, a number of potential therapeutic targets in this system is emerging. Newer agents that are more specific are being developed. The present chapter outlines the insights of the RAAS agents (classic RAAS antagonists/the new RAAS drugs), and discusses its clinical application in the combat of renal fibrosis.

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