Effect of age on the processing and import of matrix-destined mitochondrial proteins in skeletal muscle
Open accessAbstract
Deregulation of muscle mitochondrial biogenesis may explain the altered mitochondrial properties associated with aging. Maintenance of the mitochondrial network requires the continuous incorporation of nascent proteins into their subcompartments via the protein import pathway. We examined whether this pathway was impaired in muscle of aged animals, focusing on the subsarcolemmal and intermyofibrillar mitochondrial populations. Our results indicate that the import of proteins into the mitochondrial matrix was unaltered with age. Interestingly, import assays supplemented with the cytosolic fraction illustrated an attenuation of protein import, and this effect was similar between age groups. We observed a 2.5-fold increase in protein degradation in the presence of the cytosolic fraction obtained from aged animals. Thus, the reduction of mitochondrial content and/or function observed with aging may not rely on altered activity of the import pathway but rather on the availability of preproteins that are susceptible to elevated rates of degradation by cytosolic factors.
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All studies reporting an aging-related decrease in IMF mitochondrial size only assessed mitochondrial morphology in longitudinal orientation.
“Importantly, all studies reporting an aging-related decrease in IMF mitochondrial size only assessed mitochondrial morphology in longitudinal orientation.”
From Effects of Aging and Caloric Restriction on Fiber Type Composition, Mitochondrial Morphology and Dynamics in Rat Oxidative and Glycolytic Muscles (2019) · cites this paper as Huang et al., 2010
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- Authors
- Huang, J. H., Joseph, A.-M., Ljubicic, V., Iqbal, S., & Hood, D. A.
- Affiliations
- York University (CA)
- Venue
- The Journals of Gerontology Series A: Biological Sciences and Medical Sciences
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-01-02
- Volume
- 65A
- Issue
- 2
- Pages
- 138-146
- ISSN
- 1079-5006 (ISSN-L)
- 1758-535X
- PMC
- PMC6279220
- OpenAlex
- W2128890044
- Cited by
- 35
- References
- 56
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 1 · 2021: 7 · 2020: 3 · 2019: 1 · 2018: 1 · 2016: 2 · 2015: 2 · 2014: 2 · 2012: 2
- FWCI
- 1.43
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- The Journals of Gerontology Series A (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research
- National Institute on Aging (P30AG028740)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial protein import, mitochondrial matrix, aging, skeletal muscle, mitochondrial biogenesis, protein degradation, cytosolic factors, subsarcolemmal mitochondria, interfibrillar mitochondria
- MeSH terms
- Aging, Animals, Body Weight, Cytosol, Male, Mitochondria, Muscle, Ornithine Carbamoyltransferase, Protein Precursors, Rats, Inbred F344, Rats, Sprague-Dawley, Muscle, Skeletal, Molecular Chaperones, Protein Transport, Mitochondrial Proteins, Rats
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