Evidence map›Paper›PMID 42843417›Full record

ArticleBrain pathology (Zurich, Switzerland)2026

Identifying regulatory muscle processes in infantile and adult Pompe patients using a multi-omic and morphological approach.

Alexander Schaiter, Keerthika Lohanadan, Alexander Mensch, Andreas Hentschel, Angela Rosenbohm, Cornelia Kornblum, Angela Roth, Tara Procida-Kowalski, Heidrun H Krämer, Andreas Hahn and 7 more

Abstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
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

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

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

17 authors.

Alexander SchaiterInstitute of Neuropathology, Justus-Liebig-University Giessen, Giessen, Germany.
Keerthika LohanadanDepartment of Molecular Cell Biology, Institute for Cell Biology, University of Bonn, Bonn, Germany.
Alexander MenschDepartment of Neurology, University Medicine Halle, Halle (Saale), Germany.ORCID https://orcid.org/0000-0003-0089-4473
Andreas HentschelLeibnitz-Institut für Analytische Wissenschaften-ISAS-e.V., Dortmund, Germany.
Angela RosenbohmDepartment of Neurology, University Hospital Ulm, Ulm, Germany.ORCID https://orcid.org/0000-0001-9700-0338
Cornelia KornblumDepartment of Neuromuscular Diseases, Center for Neurology, University Hospital Bonn, Bonn, Germany.ORCID https://orcid.org/0000-0002-0111-7281
Angela RothInstitute of Neuropathology, Justus-Liebig-University Giessen, Giessen, Germany.
Tara Procida-KowalskiInstitute for Lung Health (ILH), Justus-Liebig-University Giessen, Giessen, Germany.ORCID https://orcid.org/0009-0004-0527-100X
Heidrun H KrämerDepartment of Neurology, Justus-Liebig-University Giessen, Giessen, Germany.ORCID https://orcid.org/0000-0003-0615-1304
Andreas HahnDepartment of Pediatric Neurology, Justus-Liebig-University Giessen, Giessen, Germany.ORCID https://orcid.org/0000-0003-0235-5211
Jörg HöhfeldDepartment of Molecular Cell Biology, Institute for Cell Biology, University of Bonn, Bonn, Germany.
Dieter O FürstDepartment of Molecular Cell Biology, Institute for Cell Biology, University of Bonn, Bonn, Germany.
Werner StenzelDepartment of Neuropathology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, RHC, Berlin, Germany.ORCID https://orcid.org/0000-0002-1143-2103
Peter F M van der VenDepartment of Molecular Cell Biology, Institute for Cell Biology, University of Bonn, Bonn, Germany.ORCID https://orcid.org/0000-0002-9750-8913
Andreas RoosDepartment of Pediatric Neurology, Centre for Neuromuscular Disorders, University Duisburg-Essen, Essen, Germany.ORCID https://orcid.org/0000-0003-2833-0928
Marek BartkuhnInstitute for Lung Health (ILH), Justus-Liebig-University Giessen, Giessen, Germany.
Anne SchänzerInstitute of Neuropathology, Justus-Liebig-University Giessen, Giessen, Germany.ORCID https://orcid.org/0000-0002-2014-2028

Funding

Bundesministerium für Forschung, Technologie und RaumfahrtEuropean Regional Development Fund'Ministerium für Kultur und Wissenschaft des Landes Nordrhein-WestfalenRegierenden Bürgermeister von Berlin-Senatskanzlei Wissenschaft und ForschungSanofi SGZ-2022-13788
6 · The paper itself

Abstract

Pompe disease is a lysosomal glycogen storage disorder caused by a deficiency of the enzyme acid alpha-glucosidase (GAA). There are two different clinical phenotypes, which are based on the age of onset, GAA variants, and residual enzyme activity. To better understand the regulation of age-dependent pathways in Pompe disease, we performed a multi-modal approach. We included mass spectrometry (MS) (liquid chromatography coupled to tandem mass spectrometry) and bulk-RNA sequencing on skeletal muscle samples from patients with late onset Pompe disease (LOPD) (n = 21) and infantile-onset Pompe disease (IOPD) (n = 11) naive to enzyme replacement therapy (ERT), IOPD patients with ERT (n = 5) and age-matched controls. The findings were verified by immunofluorescence studies and ultrastructural analysis using samples with different disease progression. We identified deregulated muscle processes in LOPD and IOPD samples, with different levels of regulation evident at the transcriptome and protein levels. Transcriptomic profiling revealed upregulation of immune processes in both Pompe subtypes, while metabolic processes were downregulated mainly in LOPD. Downregulation of transcripts associated with muscle development and myogenesis was only observed in IOPD samples. MS analysis revealed a decrease in the expression of sarcomeric proteins mainly in LOPD, while chaperone-assisted selective autophagy was altered in both Pompe subtypes. Proteins linked to vesicle trafficking and biosynthesis correlated with the degree of muscle pathology in LOPD, highlighting their role in the progression of the disease. IOPD patients treated with ERT showed normalised deregulated transcripts, though not fully back to baseline. Proteins increased with ERT were linked with mitochondrial and protein control pathways, and sarcomeric function, indicating ERT's positive effect on skeletal muscle function at the molecular level. Our findings reveal that combining a multi-omic approach, including morphological observations, enables the detection of a greater number of deregulated muscle processes, indicating both similar and distinct muscle processes in IOPD and LOPD.

Indexed as

autophagyglycogen storagelysosome storagemuscle proteomicsmuscle transcriptomicvacuolar myopathy

Identifiers

PMID42843417
PMCPMC13645463

What Socratic holds

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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 Socratic graph.