Evidence map›Paper›PMID 39199020›Full record

ArticleClinical genetics2025

Expanding the genetic landscape of Usher syndrome type IV caused by pathogenic ARSG variants.

Miriam Bauwens, Vincent De Man, Isabelle Audo, Irina Balikova, Wadih M Zein, Vasily Smirnov, Sebastian Held, Sascha Vermeer, Elke Loos, Julie Jacob and 15 more

Abstract read
In one paragraph

Article in Clinical genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
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  3. Review
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  5. 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

25 authors.

Miriam BauwensCenter for Medical Genetics, Ghent University Hospital & Department of Biomolecular Medicine, Ghent University, Ghent, Belgium.ORCID 0000-0003-0402-9006
Vincent De ManDepartment of Ophthalmology, University Hospital Leuven, Leuven, Belgium.
Isabelle AudoSorbonne Université, INSERM, CNRS, Institut de la Vision, Paris, France.ORCID 0000-0003-0698-5309
Irina BalikovaDepartment of Ophthalmology, University Hospital Leuven, Leuven, Belgium.
Wadih M ZeinOphthalmic Genetics and Visual Function Branch, NEI, NIH, Bethesda, Maryland, USA.
Vasily SmirnovSorbonne Université, INSERM, CNRS, Institut de la Vision, Paris, France.
Sebastian HeldChristian-Albrechts-University Kiel, Institute of Biochemistry, Kiel, Germany.
Sascha VermeerCenter for Human Genetics, University Hospitals Leuven, Leuven, Belgium.
Elke LoosDepartment of Otorhinolaryngology-Head and Neck Surgery, University Hospitals Leuven, Leuven, Belgium.
Julie JacobDepartment of Ophthalmology, University Hospital Leuven, Leuven, Belgium.
Ingele CasteelsDepartment of Ophthalmology, University Hospital Leuven, Leuven, Belgium.
Julie DésirCenter for Medical Genetics, Institut de Pathologie et de Génétique Gosselies, Charleroi, Belgium.
Fanny DepasseDepartment of Pediatric Ophthalmology, Queen Fabiola Children's University Hospital (HUDERF), Brussels, Belgium.
Stijn Van de SompeleCenter for Medical Genetics, Ghent University Hospital & Department of Biomolecular Medicine, Ghent University, Ghent, Belgium.
Mattias Van HeetveldeCenter for Medical Genetics, Ghent University Hospital & Department of Biomolecular Medicine, Ghent University, Ghent, Belgium.
Marieke De BruyneCenter for Medical Genetics, Ghent University Hospital & Department of Biomolecular Medicine, Ghent University, Ghent, Belgium.
Camille AndrieuCentre Hospitalier National d'Ophtalmologie des Quinze-Vingts, Centre de Référence Maladies Rares REFERET and INSERM-DGOS CIC 1423, Paris, France.
Christel CondroyerSorbonne Université, INSERM, CNRS, Institut de la Vision, Paris, France.
Aline AntonioSorbonne Université, INSERM, CNRS, Institut de la Vision, Paris, France.
Robert HufnagelOphthalmic Genetics and Visual Function Branch, NEI, NIH, Bethesda, Maryland, USA.
Ana Luísa CarvalhoMedical Genetics Unit, Centro Hospitalar e Universitário de Coimbra (CHUC), Coimbra, Portugal.
João Pedro MarquesUniversity Clinic of Medical Genetics, Faculty of Medicine, University of Coimbra (FMUC), Coimbra, Portugal.ORCID 0000-0002-1014-0483
Christina ZeitzSorbonne Université, INSERM, CNRS, Institut de la Vision, Paris, France.
Elfride De BaereCenter for Medical Genetics, Ghent University Hospital & Department of Biomolecular Medicine, Ghent University, Ghent, Belgium.
Markus DammeChristian-Albrechts-University Kiel, Institute of Biochemistry, Kiel, Germany.

Funding

Clinical ophthalmic molecular diagnostics and discoveryZIAEY000564 · NEI · NATIONAL EYE INSTITUTE · PI GUAN, BIN · 2019 to 2025
$7.9M
EJPRD19-234 Solve-RET FWO-1802220NFondation Voir et EntendreFoundation Fighting Blindness center BR-GE-0619-0761-INSERMFoundation Fighting Blindness center C-CMM-0907-0428-INSERM04IHU FOReSIGHT ANR-11-IDEX-0004-0Intramural NIH HHS ZIA EY000564LABEX LIFESENSES ANR10-LABX-65National Eye Institute, National Institutes of HealthRetina France ANR-18-IAHU-0001Retina France ANR-18-IAHU-01UNADEV in partnership with ITMO NNP/AVIESANUnion Nationale des Aveugles et Déficients VisuelsUniversiteit Gent BOF20/GOA/023
6 · The paper itself

Abstract

Usher syndrome (USH) is the most common cause of deafblindness. USH is autosomal recessively inherited and characterized by rod-cone dystrophy or retinitis pigmentosa (RP), often accompanied by sensorineural hearing loss. Variants in >15 genes have been identified as causative for clinically and genetically distinct subtypes. Among the ultra-rare and recently discovered genes is ARSG, coding for the lysosomal sulfatase Arylsulfatase G. This subtype was assigned as "USH IV" with a late onset of RP and usually late-onset progressive SNHL without vestibular involvement. Here, we describe nine new subjects and the clinical description of four cases with the USH IV phenotype bearing seven novel and two known pathogenic variants. Functional experiments indicated the complete loss of sulfatase enzymatic activity upon ectopic expression of mutated ARSG cDNA. Interestingly, we identified a homozygous missense variant, p.(Arg99His), previously described in dogs with neuronal ceroid lipofuscinosis. Our study expands the genetic landscape of ARSG-USH IV and the number of known subjects by more than 30%. These findings highlight that USH IV likely has been underdiagnosed and emphasize the need to test molecularly unresolved subjects with deafblindness syndrome. Finally, testing of ARSG should be considered for the genetic work-up of apparent isolated inherited retinal diseases.

Indexed as

Usher SyndromesAdultAgedArylsulfatasesFemaleGenetic Predisposition to DiseaseHumansMaleMiddle AgedMutationPedigreePhenotypeRetinitis PigmentosaARSG protein, humanArylsulfatasesARSGcanine variant p.(Arg99His)lysosomal sulfataseretinitis pigmentosa (RP)rod‐cone dystrophy (RCD)sensorineural hearing loss (SNHL)Usher syndrome (USH)

Identifiers

PMID39199020
PMCPMC11608847

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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.