Evidence map›Paper›PMID 41425591›Full record

ReviewFrontiers in immunology2025

Targeting ferroptosis: novel therapeutic approaches and intervention strategies for kidney diseases.

Yanfang Luo, Muyang Long, Xueqin Wu, Liuting Zeng

Erratum issuedAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
  2. Review
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  10. Gastrodin as a nephroprotective agent: Molecular docking-based modulation of oxidative stress, fibrosis, and inflammation.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
    Review
  11. Article
  12. The Role of Mitochondria in Polycystic Kidney Disease.International journal of molecular sciences · 2026
    Review
  13. Regulated cell death: a multidimensional regulatory network in the pathogenesis of renal fibrosis.Apoptosis : an international journal on programmed cell death · 2026
    Review
  14. Review
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  17. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors.

Yanfang LuoDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China.
Muyang LongDepartment of Nephrology, The Central Hospital of Shaoyang, Shaoyang, Hunan, China.
Xueqin WuDepartment of Nephrology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China.
Liuting ZengDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases (NCRC-DID), Key Laboratory of Rheumatology and Clinical Immunology, Ministry of Education, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD), characterized by structural, functional, and metabolic derangements, remains a leading cause of end-stage renal disease (ESRD) with profound global health burdens. The kidney's high oxygen demand for blood filtration renders it exquisitely sensitive to redox imbalance-an aberration common to both CKD and acute kidney injury (AKI) that, when coupled with iron dysregulation, unleashes ferroptosis: a non-apoptotic, iron-dependent form of regulated cell death driven by iron accumulation, lipid peroxidation, and antioxidant defense impairment (e.g., GPX4/SLC7A11 dysfunction), cascades to which the redox-sensitive kidney is uniquely predisposed. While ferroptosis has been linked to AKI, diabetic nephropathy (DN), and renal fibrosis, existing reviews largely suffer from two limitations: they either focus on single kidney disease entities (e.g., only AKI or DN) or reiterate generic ferroptosis mechanisms, lacking a unified pathophysiological framework that bridges acute insults, chronic fibrosis, and even renal carcinogenesis. Addressing this gap, this review offers three integrated contributions: first, it positions ferroptosis as a convergent metabolic executioner across a broader spectrum of kidney diseases-encompassing AKI, DN, renal interstitial fibrosis, systemic lupus erythematosus (SLE) nephritis, autosomal dominant polycystic kidney disease (ADPKD), renal cell carcinoma (RCC), and contrast-induced nephropathy (CIN)-while emphasizing cell type-specific vulnerabilities: tubular epithelial cells (susceptible via mitochondrial dysfunction), podocytes (via iron overload), and immune cells (e.g., neutrophils/macrophages in SLE nephritis) exhibit context-dependent ferroptosis regulation, governed by cell type-specific modulators [e.g., Nrf2 in tubules, heme oxygenase-1 (HO-1) in macrophages, and sirtuins in podocytes]. Second, it reconciles seemingly disparate findings through a redox-metabolic lens-e.g., dual roles of HO-1 (protective via heme degradation

Indexed as

FerroptosisKidney DiseasesAcute Kidney InjuryAnimalsHumansIronKidneyIronAKICKDferropotosisiron metabolismoxidative stressrenal tumortherapeutic translation

Identifiers

PMID41425591
PMCPMC12714657

What Socratic holds

Textmetadata
LicenceCC BY
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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.