Evidence map›Paper›PMID 33414422›Full record

ArticleCell death & disease2021

Snai1-induced partial epithelial-mesenchymal transition orchestrates p53-p21-mediated G2/M arrest in the progression of renal fibrosis via NF-κB-mediated inflammation.

Ruochen Qi, Jiyan Wang, Yamei Jiang, Yue Qiu, Ming Xu, Ruiming Rong, Tongyu Zhu

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

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

58 citing papers in PubMed, 119 citations in OpenAlex.

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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

7 authors at 3 institutions in 1 country.

Ruochen Qi *Department of Urology, Zhongshan Hospital, Fudan University, Shanghai, 200032, P. R. China.
Jiyan Wang *Shanghai Medical College, Fudan University, Shanghai, 200032, P.R. China.
Yamei JiangDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai, 200032, P. R. China.
Yue QiuShanghai Medical College, Fudan University, Shanghai, 200032, P.R. China.
Ming XuDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai, 200032, P. R. China.
Ruiming RongDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai, 200032, P. R. China. rong.ruiming@zs-hospital.sh.cn.
Tongyu ZhuDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai, 200032, P. R. China. zhu.tongyu@zs-hospital.sh.cn.
Fudan University · CNShanghai Institute of Organic Chemistry · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal fibrosis is the common feature of all progressive kidney diseases and exerts great burden on public health worldwide. The maladaptive repair mechanism of tubular epithelial cells, an important mediator of renal fibrogenesis, manifests with partial epithelial-mesenchymal transition (EMT) and cell cycle arrest. The aim of this study is to investigate the possible correlation between partial EMT and cell cycle arrest, and elucidate the underlying mechanism. We examined human kidney allograft samples with interstitial fibrosis and three mice renal fibrosis models, unilateral ureter obstruction (UUO), ischemia-reperfusion injury, and Adriamycin nephropathy. The partial EMT process and p53-p21 axis were elevated in both human allograft with interstitial fibrosis, as well as three mice renal fibrosis models, and showed a time-dependent increase as fibrosis progressed in the UUO model. Snai1 controlled the partial EMT process, and led to parallel changes in renal fibrosis, G2/M arrest, and inflammation. p53-p21 axis arrested cell cycle at G2/M, and prompted partial EMT and fibrosis together with inflammation. NF-κB inhibitor Bay11-7082 disrupted the reciprocal loop between Snai1-induced partial EMT and p53-p21-mediated G2/M arrest. We demonstrated the reciprocal loop between partial EMT and G2/M arrest of TECs during renal fibrogenesis and revealed NF-κB-mediated inflammatory response as the underlying mechanism. This study suggests that targeting NF-κB might be a plausible therapeutic strategy to disrupt the reciprocal loop between partial EMT and G2/M arrest, therefore alleviating renal fibrosis.

Indexed as

AnimalsDisease ProgressionEpithelial-Mesenchymal TransitionFibrosisG2 Phase Cell Cycle CheckpointsHumansInflammationKidneyMaleNF-kappa BSnail Family Transcription FactorsTumor Suppressor Protein p53NF-kappa BSNAI1 protein, humanSnail Family Transcription FactorsTumor Suppressor Protein p53

Identifiers

PMID33414422
PMCPMC7790819
OpenAlexW3121087084

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.