Evidence map›Paper›PMID 41865104›Full record

ArticleScientific reports2026

TCF4 trinucleotide repeat expansion drives distinct proteomic signatures in Fuchs endothelial corneal dystrophy.

Taichi Yuasa, Tatsuya Nakagawa, Tetsuro Honda, Go Nishiuchi, Masakazu Sato, Ayumi Tokunaga, Makiko Nakahara, Theofilos Tourtas, Ursula Schlötzer-Schrehardt, Friedrich Kruse and 8 more

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Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

18 authors.

Taichi YuasaDepartment of Biomedical Engineering, Faculty of Life and Medical Sciences, Doshisha University, Kyotanabe, 610-0394, Japan.
Tatsuya NakagawaDepartment of Biomedical Engineering, Faculty of Life and Medical Sciences, Doshisha University, Kyotanabe, 610-0394, Japan.
Tetsuro HondaDepartment of Biomedical Engineering, Faculty of Life and Medical Sciences, Doshisha University, Kyotanabe, 610-0394, Japan.
Go NishiuchiDepartment of Biomedical Engineering, Faculty of Life and Medical Sciences, Doshisha University, Kyotanabe, 610-0394, Japan.
Masakazu SatoDepartment of Biomedical Engineering, Faculty of Life and Medical Sciences, Doshisha University, Kyotanabe, 610-0394, Japan.
Ayumi TokunagaDepartment of Biomedical Engineering, Faculty of Life and Medical Sciences, Doshisha University, Kyotanabe, 610-0394, Japan.
Makiko NakaharaDepartment of Biomedical Engineering, Faculty of Life and Medical Sciences, Doshisha University, Kyotanabe, 610-0394, Japan.
Theofilos TourtasDepartment of Ophthalmology, University of Erlangen-Nürnberg, Erlangen, Germany.
Ursula Schlötzer-SchrehardtDepartment of Ophthalmology, University of Erlangen-Nürnberg, Erlangen, Germany.
Friedrich KruseDepartment of Ophthalmology, University of Erlangen-Nürnberg, Erlangen, Germany.
Prema PadmanabhanDepartment of Cornea and Refractive Surgery, Sankara Nethralaya, Chennai, India.
Amit ChatterjeeDepartment of Nanobiotechnology, Vision Research Foundation, Sankara Nethralaya, 18 College Road, Chennai, Tamil Nadu, 600 006, India.
Gajanan SatheInstitute of Bioinformatics, Bangalore, India.
Vivek GhoseInstitute of Bioinformatics, Bangalore, India.
Narayanan JanakiramanDepartment of Nanobiotechnology, Vision Research Foundation, Sankara Nethralaya, 18 College Road, Chennai, Tamil Nadu, 600 006, India.
Noriko KoizumiDepartment of Biomedical Engineering, Faculty of Life and Medical Sciences, Doshisha University, Kyotanabe, 610-0394, Japan.
Sailaja V ElchuriDepartment of Nanobiotechnology, Vision Research Foundation, Sankara Nethralaya, 18 College Road, Chennai, Tamil Nadu, 600 006, India. sailaja.elchuri@gmail.com.
Naoki OkumuraDepartment of Biomedical Engineering, Faculty of Life and Medical Sciences, Doshisha University, Kyotanabe, 610-0394, Japan. nokumura@mail.doshisha.ac.jp.

Funding

Japan Society for the Promotion of Science KAKENHI 18K09464Science and Engineering Research Board EMR/2015/000607
6 · The paper itself

Abstract

The aims of this study were to use an isogenic cell model system to investigate the proteomic consequences of TCF4 trinucleotide repeat expansion in Fuchs endothelial corneal dystrophy (FECD) and to identify potential molecular pathways contributing to disease pathogenesis. We used our previously established immortalized FECD cells (iFECD) that harbor CTG repeat expansion in TCF4 and CRISPR/Cas9 genome editing to generate an isogenic counterpart (iFECD TCF4ΔCTG) in which the expansion was deleted. Comprehensive proteomic analysis was then performed using tandem mass tag (TMT)-labeled quantitative LC-MS/MS. The resulting data were subjected to differential expression analysis, functional enrichment analysis, and protein-protein interaction network construction to elucidate the molecular impact of the CTG repeat expansion. Deletion of the CTG repeat expansion significantly altered the corneal endothelial proteome, with 90 upregulated and 111 downregulated proteins (|log

Indexed as

Fuchs' Endothelial DystrophyProteomeProteomicsTranscription Factor 4Trinucleotide Repeat ExpansionHumansProtein Interaction MapsProteomeTCF4 protein, humanTranscription Factor 4

Identifiers

PMID41865104
PMCPMC13149823

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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.