Evidence map›Paper›PMID 41904731›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2026

Exploring a plasma proteomic biosignature associated with cardiac involvement in Fabry disease.

Thi Hai Yen Nguyen, Quang Thu Nguyen, Franklin Ducatez, Abdellah Tebani, Phuoc Long Nguyen, Soumeya Bekri

Abstract read
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In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

6 authors.

Thi Hai Yen NguyenDepartment of Metabolic Biochemistry, UNIROUEN, AIMS, CHU Rouen, Referral Center for Lysosomal Diseases, Normandie University, Filière G2M, 76000, Rouen, SysMedLab, France.
Quang Thu NguyenGraduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, 333, Taoyuan, Taiwan.
Franklin DucatezDepartment of Metabolic Biochemistry, UNIROUEN, AIMS, CHU Rouen, Referral Center for Lysosomal Diseases, Normandie University, Filière G2M, 76000, Rouen, SysMedLab, France.
Abdellah TebaniDepartment of Metabolic Biochemistry, UNIROUEN, AIMS, CHU Rouen, Referral Center for Lysosomal Diseases, Normandie University, Filière G2M, 76000, Rouen, SysMedLab, France.
Phuoc Long NguyenGraduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, 333, Taoyuan, Taiwan.
Soumeya BekriDepartment of Metabolic Biochemistry, UNIROUEN, AIMS, CHU Rouen, Referral Center for Lysosomal Diseases, Normandie University, Filière G2M, 76000, Rouen, SysMedLab, France. soumeya.bekri@chu-rouen.fr.ORCID http://orcid.org/0000-0001-6184-7270

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fabry disease (FD) is an X-linked lysosomal disorder caused by a deficiency in α-galactosidase A, leading to the accumulation of globotriaosylceramide (Gb3) and lysoGb3. While this accumulation was long seen as the leading cause of symptoms, FD pathogenesis now involves complex mechanisms like autophagy dysregulation, inflammation, oxidative stress, and inter-organelle communication. Cardiovascular diseases (CVD) remain a significant reason for premature death in FD. Gaining a better understanding of cardiac pathophysiology and developing new biomarkers for early detection and monitoring in FD are still essential. In this study, we proposed an FD-CVD protein signature by analyzing the plasma proteome of 55 FD patients, including 18 with CVD and 37 without (woCVD), and 30 non-FD controls. We found 141 altered proteins in FD-CVD compared to FD-woCVD. Among them, 38 differential proteins are related to cardiometabolism. Moreover, ten proteins were identified as potential biomarkers for differentiating FD-CVD from FD-woCVD. The 10-protein signature performed well in RF and partial least squares discriminant analysis models but had limited predictive ability in support vector machine and logistic regression. Importantly, this biosignature demonstrated an ability to classify FD and non-FD controls, regardless of CVD complications, with AUCs greater than 0.90. Using a local interpretable model-agnostic explanation, the RF model interpretation revealed the classification rule for FD-woCVD and highlighted the significance of GDF15, NOS1, CCN5, CTSF, and NAAA. Our findings suggest an early indication of combined cardiac involvement in FD, paving the way for future validation studies that may ultimately inform personalized treatment before irreversible heart damage develops. KEY MESSAGES: Cardiovascular diseases (CVD) remain the leading cause of premature death in Fabry. A ten-protein signature was identified to differentiate Fabry with and without CVD. The protein signature could classify Fabry with controls regardless of CVD status.

Indexed as

Blood ProteinsCardiovascular DiseasesFabry DiseaseProteomeProteomicsAdultBiomarkersFemaleHumansMaleMiddle AgedBiomarkersBlood ProteinsProteomeBiomarkersCardiovascular diseaseFabry diseaseMachine learningProteomicsSystems biology

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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.