Evidence map›Paper›PMID 42826479›Full record

ArticleRedox biology2026

PRMT5 promotes ferroptosis in cisplatin-induced acute kidney injury through WDR5/ACSL4 pathway.

Jiawen Lin, Junxuan Fang, Tianjiao Cui, Jiaqi Xu, Wenjian Lin, Shuping Li, Yuan Sui, Zhihua Zheng, Keping Wu, Mingcheng Huang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Redox biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Jiawen LinDepartment of Nephrology, Kidney and Urology Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, Guangdong, China.
Junxuan FangDepartment of Nephrology, Kidney and Urology Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, Guangdong, China.
Tianjiao CuiDepartment of Nephrology, Kidney and Urology Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, Guangdong, China.
Jiaqi XuDepartment of Nephrology, Kidney and Urology Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, Guangdong, China.
Wenjian LinDepartment of Nephrology, Kidney and Urology Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, Guangdong, China.
Shuping LiDepartment of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, USA.
Yuan SuiMolecular and Cellular Biology Laboratory, The Salk Institute for Biological Studies, La Jolla, CA, USA.
Zhihua ZhengDepartment of Nephrology, Kidney and Urology Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, Guangdong, China. Electronic address: zhzhihua@mail.sysu.edu.cn.
Keping WuDepartment of Nephrology, Kidney and Urology Center, The Sixth Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China. Electronic address: Wukp@mail2.sysu.edu.cn.
Mingcheng HuangDepartment of Nephrology, Kidney and Urology Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, Guangdong, China. Electronic address: huangmch6@mail.sysu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epigenetic mechanisms driving the transition to ferroptosis in acute kidney injury (AKI) remain unclear. In this study, protein methyltransferase 5 (PRMT5) and its partner MEP50 were significantly upregulated in the renal tubules of AKI patients and murine models. Genetic silencing of PRMT5 via AAV-shRNA in vivo and siRNA in vitro improved renal function, attenuated mitochondrial damage, and suppressed ferroptotic tubular cell death. Mechanistically, PRMT5 promotes ACSL4 expression in a WDR5-dependent manner, facilitating tubular ferroptosis. Pharmacological inhibition of PRMT5 (GSK591) post-treatment or cloperastine hydrochloride prophylactic administration similarly improved renal function and limited ferroptotic cell death. These findings offer novel insights into the upstream epigenetic regulation of ACSL4-driven ferroptosis and suggest that PRMT5-ACSL4 axis might be a potential therapeutic target for AKI intervention.

Indexed as

Acute kidney injury (AKI)CisplatinFerroptosisLipid peroxidationProtein methyltransferase 5 (PRMT5)

Identifiers

PMID42826479
PMCPMC13659685

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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.