Evidence map›Paper›PMID 42158138›Full record

SynthesisFrontiers in medicine2026

Ferroptosis inhibition as a renoprotective strategy in cisplatin-induced acute kidney injury: multilevel meta-analysis of mechanistic biomarkers.

Burcu Yuksel, Nurullah Eryilmaz

Abstract readSystematic Review
In one paragraph

Synthesis in Frontiers in medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

2 authors.

Burcu YukselKocaeli University, İzmit, Türkiye.
Nurullah EryilmazUniversity of Bath, Bath, United Kingdom.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Cisplatin-induced acute kidney injury (CI-AKI) is a severe, dose-limiting nephrotoxicity affecting up to 30% of patients. Emerging evidence highlights ferroptosis-an iron-dependent form of regulated cell death-as a key mechanism in cisplatin-induced tubular damage. However, the overall effectiveness of various ferroptosis inhibitors remains unclear. This study aims to synthesise preclinical evidence to assess the renoprotective potential of natural and synthetic agents targeting the ferroptotic cascade. Methods: Following PRISMA 2020 guidelines, a systematic review and multilevel meta-analysis were conducted across PubMed and Web of Science. From 58 unique preclinical studies (265 effect sizes), we extracted data on renal function (BUN, SCr) and ferroptotic biomarkers (GPX4, GSH, MDA, 4-HNE, Fe Results: Both natural and synthetic interventions significantly alleviated renal dysfunction, markedly reducing BUN (Intercepts Conclusion: Inhibition of ferroptosis is a promising preclinical strategy to mitigate CI-AKI, with restoration of the System Xc-/GSH/GPX4 axis emerging as the primary mechanistic driver of renoprotection. These results provide a quantitative mechanistic consensus supporting further investigation and clinical development of ferroptosis-targeted adjuvants to widen the therapeutic window of cisplatin-based chemotherapy.

Indexed as

acute kidney injurycisplatinferroptosisglutathioneGPX4meta-analysisrenoprotection

Identifiers

PMID42158138
PMCPMC13180951

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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.