Evidence map›Paper›PMID 30121551›Full record

ArticleMolecular therapy. Nucleic acids2018

lncRNA ZEB1-AS1 Was Suppressed by p53 for Renal Fibrosis in Diabetic Nephropathy.

Juan Wang, Jian Pan, Huiling Li, Jie Long, Fang Fang, Junxiang Chen, Xuejin Zhu, Xudong Xiang, Dongshan Zhang

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.1field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 89 citations in OpenAlex.

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  16. Inhibition of PKC-δ reduce rhabdomyolysis-induced acute kidney injury.Journal of cellular and molecular medicine · 2022
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  18. The Long Noncoding RNADNA and cell biology · 2022
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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

9 authors at 2 institutions in 1 country.

Juan WangDepartment of Emergency Medicine, Second Xiangya Hospital, Central South University, Changsha, Hunan, China; Department of Nephrology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jian PanDepartment of Emergency Medicine, Second Xiangya Hospital, Central South University, Changsha, Hunan, China; Department of Nephrology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Huiling LiDepartment of Ophthalmology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jie LongDepartment of Emergency Medicine, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Fang FangDepartment of Ophthalmology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Junxiang ChenDepartment of Nephrology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xuejin ZhuDepartment of Nephrology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xudong XiangDepartment of Emergency Medicine, Second Xiangya Hospital, Central South University, Changsha, Hunan, China. Electronic address: xudongx_99@hotmail.com.
Dongshan ZhangDepartment of Emergency Medicine, Second Xiangya Hospital, Central South University, Changsha, Hunan, China; Department of Nephrology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China. Electronic address: 715653110@qq.com.
Second Xiangya Hospital of Central South University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of p53 in renal fibrosis is still controversial, and its underlying mechanisms remain not clear. Here, we showed that the pharmacological inhibition and genetic deletion of p53 in proximal tubular cells can attenuate renal dysfunction, tubular epithelial disruption, and interstitial fibrosis in db/db and STZ-induced diabetic nephrology (DN) mice. In human renal proximal tubule (human kidney 2 [HK-2]) cells, inhibition of p53 by PIF reduced the high glucose (HG)-induced extracellular matrix (ECM) accumulation and reversed the inhibitory effect of HG on mRNA expression levels of lncRNA zinc finger E-box binding homeobox1-antisense RNA 1 (ZEB1-AS1) and ZEB1. Interestingly, our results demonstrated that both lncRNA ZEB1-AS1 and ZEB1 exhibited an anti-fibrotic role, while ZEB1 is positively regulated by lncRNA ZEB1-AS1 during HG treatment. Mechanistically, lnc ZEB1-AS1 bound directly to H3K4 methyltransferase myeloid and lymphoid or mixed-lineage leukemia 1 (MLL1) and promoted H3K4me3 histone modification on ZEB1 promoter, which was reduced by HG treatment. ChIP analysis indicated the binding of p53 to the promoter region of lnc ZEB1-AS1. Furthermore, the findings were verified by the kidney biopsy samples from patients with DN. Taken all together, our results suggest that p53 may be a therapeutic target for renal fibrosis in DN.

Indexed as

diabetic nephropathylncRNA ZEB1-AS1p53ZEB1

Identifiers

PMID30121551
PMCPMC6095953
OpenAlexW2885277821

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Registered trials

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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.