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Cited by 666

The DOI matches its Crossref record; 119 of the 119 references it cites were found in a registry or an index.

TGF-β/Smad signaling in renal fibrosis

Open access
Meng, Xiao-Ming, Tang, Patrick Ming-Kuen, Li, Jun, Lan, Hui Yao·2015·Frontiers in Physiology
DOI 10.3389/fphys.2015.00082
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Abstract

TGF-β (transforming growth factor-β) is well identified as a central mediator in renal fibrosis. TGF-β initiates canonical and non-canonical pathways to exert multiple biological effects. Among them, Smad signaling is recognized as a major pathway of TGF-β signaling in progressive renal fibrosis. During fibrogenesis, Smad3 is highly activated, which is associated with the down-regulation of an inhibitory Smad7 via an ubiquitin E3-ligases-dependent degradation mechanism. The equilibrium shift between Smad3 and Smad7 leads to accumulation and activation of myofibroblasts, overproduction of ECM (extracellular matrix), and reduction in ECM degradation in the diseased kidney. Therefore, overexpression of Smad7 has been shown to be a therapeutic agent for renal fibrosis in various models of kidney diseases. In contrast, another downstream effecter of TGF-β/Smad signaling pathway, Smad2, exerts its renal protective role by counter-regulating the Smad3. Furthermore, recent studies demonstrated that Smad3 mediates renal fibrosis by down-regulating miR-29 and miR-200 but up-regulating miR-21 and miR-192. Thus, overexpression of miR-29 and miR-200 or down-regulation of miR-21 and miR-192 is capable of attenuating Smad3-mediated renal fibrosis in various mouse models of chronic kidney diseases (CKD). Taken together, TGF-β/Smad signaling plays an important role in renal fibrosis. Targeting TGF-β/Smad3 signaling may represent a specific and effective therapy for CKD associated with renal fibrosis.

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Cited by

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Metadata

Authors
Meng, X.-M., Tang, P. M.-K., Li, J., & Lan, H. Y.
Venue
Frontiers in Physiology
Publisher
Frontiers Media SA
Published
2015-03-19
Volume
6
Pages
82-82
ISSN
1664-042X (ISSN-L)
DOI
10.3389/fphys.2015.00082
OpenAlex
W2110886621
Cited by
666
References
119
FWCI
22.39
Type
journal article
Language
en
Open access
gold

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