Evidence map›Paper›PMID 40329437›Full record

ReviewRenal failure2025

Ferroptosis and renal fibrosis: mechanistic insights and emerging therapeutic targets.

Guangna Lyu, Hui Liao, Rongshan Li

Abstract readReview
In one paragraph

Review in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

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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

3 authors.

Guangna LyuThe Nephrology Department of Shanxi Provincial People's Hospital, Shanxi Medical University, Taiyuan, China.
Hui LiaoThe Drug Clinical Trial Institution of Shanxi Provincial People's Hospital, Shanxi Medical University, Taiyuan, China.
Rongshan LiThe Nephrology Department of Shanxi Provincial People's Hospital, Shanxi Medical University, Taiyuan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis is a regulated, iron-dependent form of cell death driven by lipid peroxidation and distinct from apoptosis, necroptosis, and pyroptosis. Recent studies implicate ferroptosis as a central contributor to the pathogenesis of renal fibrosis, a hallmark of chronic kidney disease associated with high morbidity and progression to end-stage renal failure. This review synthesizes current evidence linking ferroptotic signaling to fibrotic remodeling in the kidney, focusing on iron metabolism dysregulation, glutathione peroxidase 4 (GPX4) inactivation, lipid peroxide accumulation, and ferroptosis-regulatory pathways such as FSP1-CoQ10-NAD(P)H and GCH1-BH4. We detail how ferroptosis in tubular epithelial cells modulates pro-fibrotic cytokine release, macrophage recruitment, and TGF-β1-driven extracellular matrix deposition. Moreover, we explore ferroptosis as a therapeutic vulnerability in renal fibrosis, highlighting promising agents including iron chelators, GPX4 activators, anti-lipid peroxidants, and exosome-based gene delivery systems. By consolidating emerging preclinical data, this review provides a comprehensive mechanistic framework and identifies translational opportunities for targeting ferroptosis in fibrotic kidney disease.

Indexed as

FerroptosisKidneyRenal Insufficiency, ChronicAnimalsFibrosisHumansIronIron Chelating AgentsLipid PeroxidationPhospholipid Hydroperoxide Glutathione PeroxidaseSignal TransductionIronIron Chelating AgentsPhospholipid Hydroperoxide Glutathione PeroxidaseFerroptosisglutathione peroxidase 4iron metabolismlipid peroxidesreactive oxygen speciesrenal fibrosis

Identifiers

PMID40329437
PMCPMC12057793

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.