Therapeutic potential for renal fibrosis by targeting Smad3-dependent noncoding RNAs
Yue-Yu Gu1, Xu-Sheng Liu2, Hui-Yao Lan3
1State Key Laboratory of Traditional Chinese Medicine Syndrome, Department of Nephrology, Guangdong Provincial Hospital of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China; Departments of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, and Lui Che Woo Institute of Innovative Medicine, The Chinese University of Hong Kong, Hong Kong; Department of Pharmacology, School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, China; Departments of Nephrology and Pathology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, China.
Abstract:
Renal fibrosis is a characteristic hallmark of chronic kidney disease (CKD) that ultimately results in renal failure, leaving patients with few therapeutic options. TGF-β is a master regulator of renal fibrosis and mediates progressive renal fibrosis via both canonical and noncanonical signaling pathways. In the canonical Smad signaling, Smad3 is a key mediator in tissue fibrosis and mediates renal fibrosis via a number of noncoding RNAs (ncRNAs). In this regard, targeting Smad3-dependent ncRNAs may offer a specific therapy for renal fibrosis. This review highlights the significance and innovation of TGF-β/Smad3-associated ncRNAs as biomarkers and therapeutic targets in renal fibrogenesis. In addition, the underlying mechanisms of these ncRNAs and their future perspectives in the treatment of renal fibrosis are discussed.
Insights
Targeting transforming growth factor-beta (TGF-β)/Smad3-associated noncoding RNAs (ncRNAs) offers novel therapeutic strategies for chronic kidney disease (CKD) and renal fibrosis, addressing limited treatment options.
Area of Science:
- Nephrology
- Molecular Biology
- Biochemistry
Background:
- Renal fibrosis is a key feature of chronic kidney disease (CKD), leading to kidney failure.
- Transforming growth factor-beta (TGF-β) is a critical regulator of renal fibrosis through canonical and noncanonical pathways.
- Smad3 is a central mediator in TGF-β canonical signaling and drives fibrosis via noncoding RNAs (ncRNAs).
Purpose of the Study:
- To review the role of TGF-β/Smad3-associated ncRNAs in renal fibrogenesis.
- To highlight these ncRNAs as potential biomarkers and therapeutic targets for renal fibrosis.
- To discuss the mechanisms and future perspectives of these ncRNAs in treating kidney fibrosis.
Main Methods:
- Literature review focusing on TGF-β signaling, Smad3, and ncRNAs in renal fibrosis.
- Analysis of studies investigating the role of specific ncRNAs in fibrotic processes.
- Synthesis of current knowledge on mechanisms and therapeutic potential.
Main Results:
- Smad3-dependent ncRNAs are significantly involved in mediating renal fibrosis.
- These ncRNAs demonstrate potential as biomarkers for diagnosing and monitoring fibrosis.
- Targeting these ncRNAs presents a promising therapeutic avenue for renal fibrosis.
Conclusions:
- TGF-β/Smad3-associated ncRNAs are pivotal in the development of renal fibrosis.
- These ncRNAs represent innovative biomarkers and therapeutic targets for kidney fibrosis.
- Further research into their mechanisms could lead to novel treatments for CKD.
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