Potential of Modulating Aldosterone Signaling and Mineralocorticoid Receptor with microRNAs to Attenuate Diabetic Kidney Disease

Diabetic Kidney Disease (DKD) is a significant complication of diabetes and primary cause of end-stage renal disease globally. The exact mechanisms underlying DKD remain poorly understood, but multiple factors, including the renin–angiotensin–aldosterone system (RAAS), play a key role in its progres...

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Main Authors: Shinji Hagiwara, Tomohito Gohda, Phillip Kantharidis, Jun Okabe, Maki Murakoshi, Yusuke Suzuki
Format: Article
Language:English
Published: MDPI AG 2024-01-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/25/2/869
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author Shinji Hagiwara
Tomohito Gohda
Phillip Kantharidis
Jun Okabe
Maki Murakoshi
Yusuke Suzuki
author_facet Shinji Hagiwara
Tomohito Gohda
Phillip Kantharidis
Jun Okabe
Maki Murakoshi
Yusuke Suzuki
author_sort Shinji Hagiwara
collection DOAJ
description Diabetic Kidney Disease (DKD) is a significant complication of diabetes and primary cause of end-stage renal disease globally. The exact mechanisms underlying DKD remain poorly understood, but multiple factors, including the renin–angiotensin–aldosterone system (RAAS), play a key role in its progression. Aldosterone, a mineralocorticoid steroid hormone, is one of the key components of RAAS and a potential mediator of renal damage and inflammation in DKD. miRNAs, small noncoding RNA molecules, have attracted interest due to their regulatory roles in numerous biological processes. These processes include aldosterone signaling and mineralocorticoid receptor (MR) expression. Numerous miRNAs have been recognized as crucial regulators of aldosterone signaling and MR expression. These miRNAs affect different aspects of the RAAS pathway and subsequent molecular processes, which impact sodium balance, ion transport, and fibrosis regulation. This review investigates the regulatory roles of particular miRNAs in modulating aldosterone signaling and MR activation, focusing on their impact on kidney injury, inflammation, and fibrosis. Understanding the complex interaction between miRNAs and the RAAS could lead to a new strategy to target aldosterone signaling and MR activation using miRNAs. This highlights the potential of miRNA-based interventions for DKD, with the aim of enhancing kidney outcomes in individuals with diabetes.
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spelling doaj.art-668aaba9abcc490aba8470b9a75447b92024-01-29T13:55:08ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672024-01-0125286910.3390/ijms25020869Potential of Modulating Aldosterone Signaling and Mineralocorticoid Receptor with microRNAs to Attenuate Diabetic Kidney DiseaseShinji Hagiwara0Tomohito Gohda1Phillip Kantharidis2Jun Okabe3Maki Murakoshi4Yusuke Suzuki5Department of Nephrology, Juntendo University Faculty of Medicine, Tokyo 1138421, JapanDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo 1138421, JapanDepartment of Diabetes, Monash University, Melbourne, VIC 3004, AustraliaDepartment of Diabetes, Monash University, Melbourne, VIC 3004, AustraliaDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo 1138421, JapanDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo 1138421, JapanDiabetic Kidney Disease (DKD) is a significant complication of diabetes and primary cause of end-stage renal disease globally. The exact mechanisms underlying DKD remain poorly understood, but multiple factors, including the renin–angiotensin–aldosterone system (RAAS), play a key role in its progression. Aldosterone, a mineralocorticoid steroid hormone, is one of the key components of RAAS and a potential mediator of renal damage and inflammation in DKD. miRNAs, small noncoding RNA molecules, have attracted interest due to their regulatory roles in numerous biological processes. These processes include aldosterone signaling and mineralocorticoid receptor (MR) expression. Numerous miRNAs have been recognized as crucial regulators of aldosterone signaling and MR expression. These miRNAs affect different aspects of the RAAS pathway and subsequent molecular processes, which impact sodium balance, ion transport, and fibrosis regulation. This review investigates the regulatory roles of particular miRNAs in modulating aldosterone signaling and MR activation, focusing on their impact on kidney injury, inflammation, and fibrosis. Understanding the complex interaction between miRNAs and the RAAS could lead to a new strategy to target aldosterone signaling and MR activation using miRNAs. This highlights the potential of miRNA-based interventions for DKD, with the aim of enhancing kidney outcomes in individuals with diabetes.https://www.mdpi.com/1422-0067/25/2/869Diabetic Kidney DiseasemicroRNAaldosteronemineralocorticoid receptor
spellingShingle Shinji Hagiwara
Tomohito Gohda
Phillip Kantharidis
Jun Okabe
Maki Murakoshi
Yusuke Suzuki
Potential of Modulating Aldosterone Signaling and Mineralocorticoid Receptor with microRNAs to Attenuate Diabetic Kidney Disease
International Journal of Molecular Sciences
Diabetic Kidney Disease
microRNA
aldosterone
mineralocorticoid receptor
title Potential of Modulating Aldosterone Signaling and Mineralocorticoid Receptor with microRNAs to Attenuate Diabetic Kidney Disease
title_full Potential of Modulating Aldosterone Signaling and Mineralocorticoid Receptor with microRNAs to Attenuate Diabetic Kidney Disease
title_fullStr Potential of Modulating Aldosterone Signaling and Mineralocorticoid Receptor with microRNAs to Attenuate Diabetic Kidney Disease
title_full_unstemmed Potential of Modulating Aldosterone Signaling and Mineralocorticoid Receptor with microRNAs to Attenuate Diabetic Kidney Disease
title_short Potential of Modulating Aldosterone Signaling and Mineralocorticoid Receptor with microRNAs to Attenuate Diabetic Kidney Disease
title_sort potential of modulating aldosterone signaling and mineralocorticoid receptor with micrornas to attenuate diabetic kidney disease
topic Diabetic Kidney Disease
microRNA
aldosterone
mineralocorticoid receptor
url https://www.mdpi.com/1422-0067/25/2/869
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