Syntaphilin loss enhances mitochondrial axonal transport and neuromuscular junction formation in a human stem cell derived neuromuscular assembloid model

This proof-of-concept study demonstrated that enhancing mitochondrial mobility could provide a therapeutic target to prevent NMJ degeneration.

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Publication Details

Journal
Molecular Medicine
Published
2025-11-05
DOI
https://doi.org/10.1186/s10020-025-01319-x
Primary Topic
Muscle Physiology and Disorders
Type
article
Field-Weighted Citation Impact
0.00

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article

Syntaphilin loss enhances mitochondrial axonal transport and neuromuscular junction formation in a human stem cell derived neuromuscular assembloid model

Esra Özkan, David Story, Vidya Ramesh, Bhuvaneish Thangaraj Selvaraj et al.
Molecular Medicine
Muscle Physiology and Disorders
article

Syntaphilin loss enhances mitochondrial axonal transport and neuromuscular junction formation in a human stem cell derived neuromuscular assembloid model

Esra Özkan, David Story, Vidya Ramesh, Bhuvaneish Thangaraj Selvaraj, Nhan T. Pham, Andrea Salzinger, Siddharthan Chandran, Jyoti Nanda, Karen Burr
article en

Abstract

This proof-of-concept study demonstrated that enhancing mitochondrial mobility could provide a therapeutic target to prevent NMJ degeneration.

Molecular MedicineVol. 31(1)
MRC Centre for Regenerative Medicine (GB), UK Dementia Research Institute (GB), University of Edinburgh (GB)
Humane Research Trust, European Commission, Universiteit Leiden, Leids Universitair Medisch Centrum, UK Dementia Research Institute, Medical Research Council
Openalex Percentile: Top 71%
Muscle Physiology and Disorders
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Syntaphilin loss enhances mitochondrial axonal transport and neuromuscular junction formation in a human stem cell derived neuromuscular assembloid model — Esra Özkan, David Story, et al. · Molecular Medicine (2025) | TGRS Research Map | TGRS