Loading...
Muscling in on mitochondrial sexual dimorphism; role of mitochondrial dimorphism in skeletal muscle health and disease
Nye, Gareth Lightfoot, Adam Sakellariou, Giorgos Degans, Hans
Nye, Gareth
Lightfoot, Adam
Sakellariou, Giorgos
Degans, Hans
Advisors
Editors
Other Contributors
EPub Date
Publication Date
2017-07-07
Submitted Date
Collections
Other Titles
Abstract
Mitochondria are no longer solely regarded as the cellular powerhouse; instead, they are
now implicated in mediating a wide-range of cellular processes, in the context of health
and disease. A recent article in Clinical Science, Ventura-Clapier et al. highlights the role
of sexual dimorphism in mitochondrial function in health and disease. However, we feel
the authors have overlooked arguably one of the most mitochondria-rich organs in skeletal
muscle. Many studies have demonstrated that mitochondria have a central role in mediating the pathogenesis of myopathologies. However, the impact of sexual dimorphism in this
context is less clear, with several studies reporting conflicting observations. For instance in
ageing studies, a rodent model reported female muscles have higher antioxidant capacity
compared with males; in contrast, human studies demonstrate no sex difference in mitochondrial bioenergetics and oxidative damage. These divergent observations highlight the
importance of considering models and methods used to examine mitochondrial function,
when interpreting these data. The use of either isolated or intact mitochondrial preparations
in many studies appears likely to be a source of discord, when comparing many studies.
Overall, it is now clear that more research is needed to determine if sexual dimorphism is a
contributing factor in the development of myopathologies.
Citation
Nye, G., Sakellariou, G., Degens, H., & Lightfoot, A. (2017). Muscling in on mitochondrial sexual dimorphism; role of mitochondrial dimorphism in skeletal muscle health and disease. Clinical Science, 131(15), 1919-1922.
Publisher
Portland Press
Journal
Clinical Science
Research Unit
DOI
10.1042/CS20160940
PubMed ID
PubMed Central ID
Type
Article
Language
en
Description
Series/Report no.
ISSN
0143-5221
EISSN
1470-8736