Evidence map›Paper›PMID 34226503›Full record

ArticleCell death discovery2021

DNA demethylase Tet2 suppresses cisplatin-induced acute kidney injury.

Yinwu Bao, Mengqiu Bai, Huanhuan Zhu, Yuan Yuan, Ying Wang, Yunjing Zhang, Junni Wang, Xishao Xie, Xi Yao, Jianhua Mao and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 22 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

14 authors at 4 institutions in 1 country.

Yinwu Bao *The Kidney Disease Center, the First Affiliated Hospital, Zhejiang University School of Medicine; Institute of Nephrology, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Hangzhou, Zhejiang Province, 310003, China.
Mengqiu Bai *The Kidney Disease Center, the First Affiliated Hospital, Zhejiang University School of Medicine; Institute of Nephrology, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Hangzhou, Zhejiang Province, 310003, China.
Huanhuan Zhu *The Kidney Disease Center, the First Affiliated Hospital, Zhejiang University School of Medicine; Institute of Nephrology, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Hangzhou, Zhejiang Province, 310003, China.
Yuan YuanThe Kidney Disease Center, the First Affiliated Hospital, Zhejiang University School of Medicine; Institute of Nephrology, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Hangzhou, Zhejiang Province, 310003, China.
Ying WangDepartment of Nephrology, The Fourth Affiliated Hospital, Zhejiang University School of Medicine, Jinhua, 322000, China.
Yunjing ZhangDepartment of Nephrology, The Fourth Affiliated Hospital, Zhejiang University School of Medicine, Jinhua, 322000, China.
Junni WangThe Kidney Disease Center, the First Affiliated Hospital, Zhejiang University School of Medicine; Institute of Nephrology, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Hangzhou, Zhejiang Province, 310003, China.
Xishao XieThe Kidney Disease Center, the First Affiliated Hospital, Zhejiang University School of Medicine; Institute of Nephrology, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Hangzhou, Zhejiang Province, 310003, China.
Xi YaoThe Kidney Disease Center, the First Affiliated Hospital, Zhejiang University School of Medicine; Institute of Nephrology, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Hangzhou, Zhejiang Province, 310003, China.
Jianhua MaoDepartment of Nephrology, Children's Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.
Xianghui FuDivision of Endocrinology and Metabolism, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center of Biotherapy, Chengdu, 610041, China.
Jianghua ChenThe Kidney Disease Center, the First Affiliated Hospital, Zhejiang University School of Medicine; Institute of Nephrology, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Hangzhou, Zhejiang Province, 310003, China. chenjianghua@zju.edu.cn.
Yi YangThe Kidney Disease Center, the First Affiliated Hospital, Zhejiang University School of Medicine; Institute of Nephrology, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Hangzhou, Zhejiang Province, 310003, China. yangyixk@zju.edu.cn.
Weiqiang LinDepartment of Nephrology, The Fourth Affiliated Hospital, Zhejiang University School of Medicine, Jinhua, 322000, China. wlin@zju.edu.cn.ORCID http://orcid.org/0000-0002-2171-8009
Zhejiang Center for Disease Control and Prevention · CNZhejiang University · CNChildren's Hospital of Zhejiang University · CNSichuan University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81670651National Natural Science Foundation of China (National Science Foundation of China) 81770752National Natural Science Foundation of China (National Science Foundation of China) 81970573National Natural Science Foundation of China (National Science Foundation of China) 82000637
6 · The paper itself

Abstract

Demethylase Tet2 plays a vital role in the immune response. Acute kidney injury (AKI) initiation and maintenance phases are marked by inflammatory responses and leukocyte recruitment in endothelial and tubular cell injury processes. However, the role of Tet2 in AKI is poorly defined. Our study determined the degree of renal tissue damage associated with Tet2 gene expression levels in a cisplatin-induced AKI mice model. Tet2-knockout (KO) mice with cisplatin treatment experienced severe tubular necrosis and dilatation, inflammation, and AKI markers' expression levels than the wild-type mice. In addition, the administration of Tet2 plasmid protected Tet2-KO mice from cisplatin-induced nephrotoxicity, but not Tet2-catalytic-dead mutant. Tet2 KO was associated with a change in metabolic pathways like retinol, arachidonic acid, linolenic acid metabolism, and PPAR signaling pathway in the cisplatin-induced mice model. Tet2 expression is also downregulated in other AKI mice models and clinical samples. Thus, our results indicate that Tet2 has a renal protective effect during AKI by regulating metabolic and inflammatory responses through the PPAR signaling pathway.

Identifiers

PMID34226503
PMCPMC8257623
OpenAlexW3179183549

What OpenQuestion holds

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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.