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Role of non-classical renin-angiotensin system axis in renal fibrosis
1Institute of Nephrology, Department of Affiliated Zhongda Hospital, Southeast University Nanjing, China.
Abstract:
The renin-angiotensin system (RAS) is a major regulator of renal fibrosis. Besides the classical renin/Angiotensin-converting enzyme (ACE)/angiotensin II (Ang II)/AT1 and AT2 axis, multiple new axes have been recently described. The new members have added new dimensions to RAS, including the ACE2/Ang(1-7)/Mas receptor axis, the prorenin/(pro)renin receptor(PRR)/intracelluar pathway axis, and the Angiotensin A (Ang A), alamandine-Mas-related G protein coupled receptor D(MrgD) axis. This review summarized recent studies regarding role of the non-classical RAS axis in renal fibrosis, and its possible implications to the intervention of progression of chronic kidney disease.
Insights
The renin-angiotensin system (RAS) regulates kidney fibrosis through classical and newly discovered pathways. Understanding these non-classical RAS axes offers new strategies for treating chronic kidney disease progression.
Area of Science:
- Nephrology
- Cardiovascular Research
- Molecular Biology
Background:
- The renin-angiotensin system (RAS) is crucial for regulating renal fibrosis.
- Classical RAS axis involves renin/ACE/Ang II/AT1 and AT2.
- Emerging non-classical RAS axes significantly impact renal function.
Purpose of the Study:
- To review recent studies on non-classical RAS axes in renal fibrosis.
- To explore the implications of these axes for chronic kidney disease (CKD) intervention.
- To provide a comprehensive overview of novel RAS pathways.
Main Methods:
- Literature review of recent scientific studies.
- Analysis of research on non-classical RAS components.
- Synthesis of findings on renal fibrosis and CKD progression.
Main Results:
- Identified ACE2/Ang(1-7)/Mas receptor axis.
- Described prorenin/(pro)renin receptor (PRR)/intracellular pathway axis.
- Highlighted Angiotensin A (Ang A)/alamandine-Mas-related G protein coupled receptor D (MrgD) axis.
- Demonstrated the role of these axes in renal fibrosis.
Conclusions:
- Non-classical RAS axes represent novel regulators of renal fibrosis.
- Targeting these pathways may offer new therapeutic strategies for CKD.
- Further research into these axes is essential for advancing kidney disease treatment.
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