Evidence map›Paper›PMID 39990892›Full record

ArticleKidney international reports2025

Fabry Disease Podocytes Reveal Ferroptosis as a Potential Regulator of Cell Pathology.

Andrea F Wise, Igaa Ari Krisnadevi, Shoni Bruell, Han-Chung Lee, Tejasvini Bhuvan, Andrew J Kassianos, Sheetal Saini, Xiangju Wang, Helen G Healy, Elizabeth Ling Qian and 5 more

Abstract read
In one paragraph

Article in Kidney international reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Review
  2. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
    Article
  3. Article
  4. Pathogenic mechanisms in Fabry disease.Frontiers in medicine · 2026
    Review
  5. Review
  6. Review
  7. 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

15 authors.

Andrea F WiseDepartment of Pharmacology, Monash University, Clayton, Victoria, Australia.
Igaa Ari KrisnadeviDepartment of Pharmacology, Monash University, Clayton, Victoria, Australia.
Shoni BruellDepartment of Pharmacology, Monash University, Clayton, Victoria, Australia.
Han-Chung LeeDepartment of Biochemistry and Molecular Biology, Monash Proteomics and Metabolomics Platform, Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
Tejasvini BhuvanAnatomy and Developmental Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
Andrew J KassianosPathology Queensland at Royal Brisbane and Women's Hospital, Queensland Health, Queensland, Australia.
Sheetal SainiDepartment of Pharmacology, Monash University, Clayton, Victoria, Australia.
Xiangju WangPathology Queensland at Royal Brisbane and Women's Hospital, Queensland Health, Queensland, Australia.
Helen G HealyPathology Queensland at Royal Brisbane and Women's Hospital, Queensland Health, Queensland, Australia.
Elizabeth Ling QianNovo Nordisk Foundation Center for Stem Cell Medicine, Murdoch Children's Research Institute, Royal Children's Hospital, Parkville, Victoria, Australia.
David A ElliotAustralian Regenerative Medicine Institute, Monash University, Clayton, Victoria, Australia.
Joel R SteeleDepartment of Biochemistry and Molecular Biology, Monash Proteomics and Metabolomics Platform, Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
Maria FullerGenetics and Molecular Pathology, South Australia Pathology at Women's and Children's Hospital and Adelaide Medical School and School of Biological Sciences, University of Adelaide, South Australia, Australia.
Kathleen M NichollsDepartment of Nephrology, The Royal Melbourne Hospital and Department of Medicine, University of Melbourne, Parkville, Australia.
Sharon D RicardoDepartment of Pharmacology, Monash University, Clayton, Victoria, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Fabry disease (FD) results from pathogenic Methods: iPSCs were derived from patients with FD with Results: Podocytes derived from patients with FD exhibited expression of podocyte-specific markers and morphological features of FD. Reduced α-Gal A activity was observed in FD iPSC-derived podocytes along with the accumulation of Gb3. Proteomic profiling revealed distinct proteomic signatures between control and iPSC-derived podocytes from a patient with FD, with apparent variations among FD lines, highlighting Conclusion: These findings underscore the heterogeneity of FD and, for the first time, implicate ferroptosis as a potential common pathway driving its pathology.

Indexed as

ALOX15Fabry nephropathyGb3 accumulationGLA variantsinduced pluripotent stem cellsα-Gal A deficiency

Identifiers

PMID39990892
PMCPMC11843119

What OpenQuestion holds

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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 OpenQuestion graph.