ReviewDisease models & mechanisms2026
Modeling Fabry nephropathy: insights from experimental systems towards precision nephrology.
Review in Disease models & mechanisms, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Impaired fatty acid metabolism in AKI: experimental evidence - a narrative review.BMC nephrology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fabry nephropathy is a major cause of kidney failure in Fabry disease, caused by pathogenic GLA variants that reduce α-galactosidase A activity and lead to globotriaosylceramide (Gb3) accumulation. In recent years, rapid advances in experimental modeling and emerging therapeutic strategies have dramatically reshaped understanding and treatment prospects for Fabry nephropathy. Experimental models - including cellular systems, patient-derived kidney organoids, and animal models such as zebrafish, Drosophila, mice and rats - have been pivotal in elucidating classic Gb3-dependent and novel Gb3-independent pathogenic mechanisms. These insights challenge the traditional Gb3-centric paradigm by highlighting other contributors, such as its metabolite lyso-Gb3, as well as α-synuclein accumulation and endothelial dysfunction. Despite established therapies for Fabry nephropathy, such as enzyme replacement and pharmacological chaperones, disease progression remains a clinical challenge, underscoring the urgent need for deeper mechanistic understanding and precision medicine approaches. This timely Review summarizes diverse model systems' unique strengths, limitations and translational potential to guide future research and therapeutic development for this complex disease.
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Registered trials
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.