Evidence map›Paper›PMID 36692085›Full record

ArticleRedox report : communications in free radical research2023

Glutathione metabolism rewiring protects renal tubule cells against cisplatin-induced apoptosis and ferroptosis.

Xing-Qiang Dong, Li-Kai Chu, Xu Cao, Qian-Wei Xiong, Yi-Ming Mao, Ching-Hsien Chen, Yun-Li Bi, Jun Liu, Xiang-Ming Yan

Abstract read
In one paragraph

Article in Redox report : communications in free radical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

29 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  20. Involvement of α-klotho in growth hormone (GH) signaling.Journal of clinical biochemistry and nutrition · 2024
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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.

Xing-Qiang DongDepartment of Urology, Children's Hospital of Soochow University, Suzhou, People's Republic of China.
Li-Kai ChuDepartment of Urology, Children's Hospital of Soochow University, Suzhou, People's Republic of China.
Xu CaoDepartment of Urology, Children's Hospital of Soochow University, Suzhou, People's Republic of China.
Qian-Wei XiongDepartment of Urology, Children's Hospital of Soochow University, Suzhou, People's Republic of China.
Yi-Ming MaoDepartment of Thoracic Surgery, Suzhou Kowloon Hospital, Shanghai Jiao Tong University School of Medicine, Suzhou, People's Republic of China.
Ching-Hsien ChenDepartment of Internal Medicine, Division of Nephrology, University of California Davis, Davis, CA, USA.
Yun-Li BiDepartment of Urology, Children's Hospital of Soochow University, Suzhou, People's Republic of China.
Jun LiuDepartment of Urology, Children's Hospital of Soochow University, Suzhou, People's Republic of China.ORCID 0000-0002-0917-7449
Xiang-Ming YanDepartment of Urology, Children's Hospital of Soochow University, Suzhou, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal proximal tubular cells are highly vulnerable to different types of assaults during filtration and reabsorption, leading to acute renal dysfunction and eventual chronic kidney diseases (CKD). The chemotherapeutic drug cisplatin elicits cytotoxicity causing renal tubular cell death, but its executing mechanisms of action are versatile and elusive. Here, we show that cisplatin induces renal tubular cell apoptosis and ferroptosis by disrupting glutathione (GSH) metabolism. Upon cisplatin treatment, GSH metabolism is impaired leading to GSH depletion as well as the execution of mitochondria-mediated apoptosis and lipid oxidation-related ferroptosis through activating IL6/JAK/STAT3 signaling. Inhibition of JAK/STAT3 signaling reversed cell apoptosis and ferroptosis in response to cisplatin induction. Using a cisplatin-induced acute kidney injury (CAKI) mouse model, we found that inhibition of JAK/STAT3 significantly mitigates cisplatin nephrotoxicity with a reduced level of serum BUN and creatinine as well as proximal tubular distortion. In addition, the GSH booster baicalein also reclaims cisplatin-induced renal tubular cell apoptosis and ferroptosis as well as the

Indexed as

Acute Kidney InjuryFerroptosisAnimalsApoptosisCisplatinGlutathioneKidneyMiceCisplatinGlutathioneAcute kidney injuryapoptosisBaicaleinCisplatinferroptosisGlutathione metabolismJAK/STAT3renal tubular

Identifiers

PMID36692085
PMCPMC9879199

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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.