<i>Sucla2</i> Knock‐Out in Skeletal Muscle Yields Mouse Model of Mitochondrial Myopathy With Muscle Type–Specific Phenotypes
SUCLA2 loss within murine skeletal muscle yields a model of SCS-deficient mitochondrial myopathy with reduced body weight, muscle weakness and exercise intolerance. Physiological and morphological analyses of hindlimb muscles showed remarkable differences in ex vivo function and cellular consequences between the EDL and SOL muscles, with SOL muscles significantly more impacted by Sucla2 inactivation. This novel model will provide an invaluable tool for investigations of muscle-specific and fibre type-specific pathogenic mechanisms to better understand SCS-deficient myopathy.
Authors
- Marcus Miller
- Chunhai Hao (ORCID: https://orcid.org/0000-0002-6952-2232)
- Brett H. Graham (ORCID: https://orcid.org/0000-0001-8451-8154)
- Patrick J. Gillespie
- M. Lancaster (ORCID: https://orcid.org/0000-0002-8501-9282)
- Catalina Matias
- Paul S. Hafen (ORCID: https://orcid.org/0000-0002-7023-1563)
- Timothy Meyer (ORCID: https://orcid.org/0000-0003-0066-3392)
- Jeffrey J. Brault (ORCID: https://orcid.org/0000-0003-3503-0528)
- Kathryn D. Fischer
- David L. McKinzie (ORCID: https://orcid.org/0000-0002-4115-3316)
- Andrew Law
Institutions
- Indiana University School of Medicine
- Indiana University – Purdue University Indianapolis (US)
- Indiana University – Purdue University Columbus (US)
Publication Details
- Journal
- Journal of Cachexia Sarcopenia and Muscle
- Published
- 2024-10-31
- DOI
- https://doi.org/10.1002/jcsm.13617
- Citations
- 3
- Primary Topic
- Mitochondrial Function and Pathology
- Type
- article
- Field-Weighted Citation Impact
- 0.70
Funders
- National Institutes of Health
- School of Medicine, Indiana University