Therapeutic potential for renal fibrosis by targeting Smad3-dependent noncoding RNAs

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 pat...

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Bibliographic Details
Published in:Molecular therapy Vol. 32; no. 2; p. 313
Main Authors: Gu, Yue-Yu, Liu, Xu-Sheng, Lan, Hui-Yao
Format: Journal Article
Language:English
Published: United States 07.02.2024
Subjects:
Fibrosis
Humans
Kidney - metabolism
Renal Insufficiency, Chronic - genetics
Renal Insufficiency, Chronic - metabolism
Renal Insufficiency, Chronic - therapy
RNA, Untranslated - genetics
RNA, Untranslated - metabolism
Smad3 Protein - genetics
Smad3 Protein - metabolism
Transforming Growth Factor beta - genetics
Transforming Growth Factor beta - metabolism
TGF-β
Smad3
noncoding RNAs
renal fibrosis
therapy
ISSN:1525-0024, 1525-0024
Online Access:Get more information
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Summary: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.
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ObjectType-Review-3
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ISSN:1525-0024
1525-0024
DOI:10.1016/j.ymthe.2023.12.009