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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Vydáno v:Molecular therapy Ročník 32; číslo 2; s. 313
Hlavní autoři: Gu, Yue-Yu, Liu, Xu-Sheng, Lan, Hui-Yao
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 07.02.2024
Témata:
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
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Shrnutí: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.
Bibliografie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
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ISSN:1525-0024
1525-0024
DOI:10.1016/j.ymthe.2023.12.009