Evidence map›Paper›PMID 25852569›Full record

ReviewFrontiers in physiology2015

TGF-β/Smad signaling in renal fibrosis.

Xiao-Ming Meng, Patrick Ming-Kuen Tang, Jun Li, Hui Yao Lan

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 399 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
399citing papers in PubMed, 2 pooled it
26.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

399 citing papers in PubMed, 2 syntheses or guidelines pooled it, 640 citations in OpenAlex.

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  16. [Mesothelial impairment induced by peritoneal dialysis and its potential protective strategies].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2026
    Review
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339 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Xiao-Ming MengSchool of Pharmacy, Anhui Medical University Hefei, China.
Patrick Ming-Kuen TangDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong Hong Kong, China ; Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong Hong Kong, China.
Jun LiSchool of Pharmacy, Anhui Medical University Hefei, China.
Hui Yao LanDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong Hong Kong, China ; Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong Hong Kong, China ; Shenzhen Research Institute, The Chinese University of Hong Kong Shenzhen, China.
Anhui Medical University · CNChinese University of Hong Kong · CNChinese University of Hong Kong, Shenzhen · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

mechanismsrenal fibrosisSmads mediatorsTGF-ßtherapeutics

Identifiers

PMID25852569
PMCPMC4365692
OpenAlexW2110886621

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.