Evidence map›Paper›PMID 31996668›Full record

ArticleCell death & disease2020

VDR activation attenuate cisplatin induced AKI by inhibiting ferroptosis.

Zhaoxin Hu, Hao Zhang, Bin Yi, Shikun Yang, Jun Liu, Jing Hu, Jianwen Wang, Ke Cao, Wei Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
151citing papers in PubMed, 3 pooled it
17.8field-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

151 citing papers in PubMed, 3 syntheses or guidelines pooled it, 264 citations in OpenAlex.

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  4. Article
  5. In ovo injection of vitamin DPoultry science · 2026
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  7. ERM Inhibition Confers Ferroptosis Resistance through ROS-Induced NRF2 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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91 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

9 authors at 1 institution in 1 country.

Zhaoxin HuDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan Province, China.
Hao ZhangDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan Province, China. zhanghaoliaoqing@163.com.
Bin YiDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan Province, China.
Shikun YangDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan Province, China.ORCID http://orcid.org/0000-0002-6552-0176
Jun LiuDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan Province, China.
Jing HuDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan Province, China.
Jianwen WangDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan Province, China.
Ke CaoDepartment of Oncology, The Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan Province, China.ORCID http://orcid.org/0000-0001-5392-2306
Wei ZhangDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha, 410013, Hunan Province, China. weizhangxy@126.com.ORCID http://orcid.org/0000-0001-8679-6713
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our preliminary work has revealed that vitamin D receptor (VDR) activation is protective against cisplatin induced acute kidney injury (AKI). Ferroptosis was recently reported to be involved in AKI. Here in this study, we investigated the internal relation between ferroptosis and the protective effect of VDR in cisplatin induced AKI. By using ferroptosis inhibitor ferrostatin-1 and measurement of ferroptotic cell death phenotype in both in vivo and in vitro cisplatin induced AKI model, we observed the decreased blood urea nitrogen, creatinine, and tissue injury by ferrostatin-1, hence validated the essential involvement of ferroptosis in cisplatin induced AKI. VDR agonist paricalcitol could both functionally and histologically attenuate cisplatin induced AKI by decreasing lipid peroxidation (featured phenotype of ferroptosis), biomarker 4-hydroxynonenal (4HNE), and malondialdehyde (MDA), while reversing glutathione peroxidase 4 (GPX4, key regulator of ferroptosis) downregulation. VDR knockout mouse exhibited much more ferroptotic cell death and worsen kidney injury than wild type mice. And VDR deficiency remarkably decreased the expression of GPX4 under cisplatin stress in both in vivo and in vitro, further luciferase reporter gene assay showed that GPX4 were target gene of transcription factor VDR. In addition, in vitro study showed that GPX4 inhibition by siRNA largely abolished the protective effect of paricalcitol against cisplatin induced tubular cell injury. Besides, pretreatment of paricalcitol could also alleviated Erastin (an inducer of ferroptosis) induced cell death in HK-2 cell. These data suggested that ferroptosis plays an important role in cisplatin induced AKI. VDR activation can protect against cisplatin induced renal injury by inhibiting ferroptosis partly via trans-regulation of GPX4.

Indexed as

Acute Kidney InjuryAldehydesAnimalsAntineoplastic AgentsCell DeathCell LineCisplatinCreatinineCyclohexylaminesErgocalciferolsFerroptosisGlutathione PeroxidaseHumansLipid PeroxidationMaleMalondialdehyde4-hydroxy-2-nonenalAldehydesAntineoplastic AgentsCisplatinCreatinineCyclohexylamineserastinErgocalciferolsferrostatin-1Glutathione PeroxidaseMalondialdehydeparicalcitolPhenylenediaminesPiperazinesReceptors, CalcitriolRNA, Small Interfering

Identifiers

PMID31996668
PMCPMC6989512
OpenAlexW3003370181

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.