Universal Proteomic Signature After Exercise‐Induced Muscle Injury in Muscular Dystrophies
ABSTRACT Objective Several neuromuscular disorders (NMDs) are characterized by progressive muscle damage and are marked by the elevation of circulating muscle proteins from activity‐related injury. Despite a diverse array of genetic drivers, many NMDs share similar patterns of exercise intolerance a...
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| Format: | Article |
| Language: | English |
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Wiley
2025-05-01
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| Series: | Annals of Clinical and Translational Neurology |
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| Online Access: | https://doi.org/10.1002/acn3.70035 |
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| author | Mads G. Stemmerik Benjamin Barthel Nanna R. Andersen Sofie V. Skriver Alan J. Russell John Vissing |
| author_facet | Mads G. Stemmerik Benjamin Barthel Nanna R. Andersen Sofie V. Skriver Alan J. Russell John Vissing |
| author_sort | Mads G. Stemmerik |
| collection | DOAJ |
| description | ABSTRACT Objective Several neuromuscular disorders (NMDs) are characterized by progressive muscle damage and are marked by the elevation of circulating muscle proteins from activity‐related injury. Despite a diverse array of genetic drivers, many NMDs share similar patterns of exercise intolerance and higher concentrations of muscle injury proteins relative to unaffected individuals. While the interplay between the nature of the muscle injury and the specific genetic driver is poorly understood, the similarities exhibited by various NMDs suggest that a common proteomic signature of muscle injury may exist. Methods We used an established exercise challenge and the SOMAscan proteomics platform to study the baseline and post‐exercise proteomic profiles in a cross‐sectional study of three different muscular dystrophies: Becker muscular dystrophy (BMD) and limb girdle muscular dystrophy types R9 and R12. Results Our Results Uncover a Common Signature of Circulating Proteins That Are Elevated in all Three Myopathies, Some of Which Are Further Elevated by Exercise in Becker Muscular Dystrophy and Limb Girdle Muscular Dystrophy Type R9, and Others That Are Not Responsive to Exercise. Interpretation Interestingly, these two signatures exhibit opposing trajectories with age in a larger cross‐sectional cohort of BMD individuals. This research represents a first step toward defining an annotated protein signature coupled with activity‐injury, a defining pathophysiological feature of many myopathies. |
| format | Article |
| id | doaj-art-6a2b91cc0d4e4f9db2e3a57315f9a439 |
| institution | OA Journals |
| issn | 2328-9503 |
| language | English |
| publishDate | 2025-05-01 |
| publisher | Wiley |
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| series | Annals of Clinical and Translational Neurology |
| spelling | doaj-art-6a2b91cc0d4e4f9db2e3a57315f9a4392025-08-20T01:52:39ZengWileyAnnals of Clinical and Translational Neurology2328-95032025-05-01125998101110.1002/acn3.70035Universal Proteomic Signature After Exercise‐Induced Muscle Injury in Muscular DystrophiesMads G. Stemmerik0Benjamin Barthel1Nanna R. Andersen2Sofie V. Skriver3Alan J. Russell4John Vissing5Copenhagen Neuromuscular Center, Department of Neurology Rigshospitalet, University of Copenhagen Copenhagen DenmarkEdgewise Therapeutics Boulder Colorado USACopenhagen Neuromuscular Center, Department of Neurology Rigshospitalet, University of Copenhagen Copenhagen DenmarkCopenhagen Neuromuscular Center, Department of Neurology Rigshospitalet, University of Copenhagen Copenhagen DenmarkEdgewise Therapeutics Boulder Colorado USACopenhagen Neuromuscular Center, Department of Neurology Rigshospitalet, University of Copenhagen Copenhagen DenmarkABSTRACT Objective Several neuromuscular disorders (NMDs) are characterized by progressive muscle damage and are marked by the elevation of circulating muscle proteins from activity‐related injury. Despite a diverse array of genetic drivers, many NMDs share similar patterns of exercise intolerance and higher concentrations of muscle injury proteins relative to unaffected individuals. While the interplay between the nature of the muscle injury and the specific genetic driver is poorly understood, the similarities exhibited by various NMDs suggest that a common proteomic signature of muscle injury may exist. Methods We used an established exercise challenge and the SOMAscan proteomics platform to study the baseline and post‐exercise proteomic profiles in a cross‐sectional study of three different muscular dystrophies: Becker muscular dystrophy (BMD) and limb girdle muscular dystrophy types R9 and R12. Results Our Results Uncover a Common Signature of Circulating Proteins That Are Elevated in all Three Myopathies, Some of Which Are Further Elevated by Exercise in Becker Muscular Dystrophy and Limb Girdle Muscular Dystrophy Type R9, and Others That Are Not Responsive to Exercise. Interpretation Interestingly, these two signatures exhibit opposing trajectories with age in a larger cross‐sectional cohort of BMD individuals. This research represents a first step toward defining an annotated protein signature coupled with activity‐injury, a defining pathophysiological feature of many myopathies.https://doi.org/10.1002/acn3.70035exercisemuscular dystrophyproteomics |
| spellingShingle | Mads G. Stemmerik Benjamin Barthel Nanna R. Andersen Sofie V. Skriver Alan J. Russell John Vissing Universal Proteomic Signature After Exercise‐Induced Muscle Injury in Muscular Dystrophies Annals of Clinical and Translational Neurology exercise muscular dystrophy proteomics |
| title | Universal Proteomic Signature After Exercise‐Induced Muscle Injury in Muscular Dystrophies |
| title_full | Universal Proteomic Signature After Exercise‐Induced Muscle Injury in Muscular Dystrophies |
| title_fullStr | Universal Proteomic Signature After Exercise‐Induced Muscle Injury in Muscular Dystrophies |
| title_full_unstemmed | Universal Proteomic Signature After Exercise‐Induced Muscle Injury in Muscular Dystrophies |
| title_short | Universal Proteomic Signature After Exercise‐Induced Muscle Injury in Muscular Dystrophies |
| title_sort | universal proteomic signature after exercise induced muscle injury in muscular dystrophies |
| topic | exercise muscular dystrophy proteomics |
| url | https://doi.org/10.1002/acn3.70035 |
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