Abstract |
The loss of muscle mass and strength with aging, referred to as sarcopenia, is a prevalent condition among the elderly. Although the molecular mechanisms underlying sarcopenia are unclear, evidence suggests that an age-related acceleration of myocyte loss via apoptosis might be responsible for muscle perfomance decline. Interestingly, sarcopenia has been associated to a deficit of sex hormones which decrease upon aging. The skeletal muscle ability to repair and regenerate itself would not be possible without satellite cells, a subpopulation of cells that remain quiescent throughout life. They are activated in response to stress, enabling them to guide skeletal muscle regeneration. Thus, these cells could be a key factor to overcome sarcopenia. Of importance, satellite cells are 17β-estradiol (E2) and testosterone (T) targets. In this review, we summarize potential mechanisms through which these hormones regulate satellite cells activation during skeletal muscle regeneration in the elderly. The advance in its understanding will help to the development of potential therapeutic agents to alleviate and treat sarcopenia and other related myophaties.
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Authors | Anabela La Colla, Lucía Pronsato, Lorena Milanesi, Andrea Vasconsuelo |
Journal | Ageing research reviews
(Ageing Res Rev)
Vol. 24
Issue Pt B
Pg. 166-77
(Nov 2015)
ISSN: 1872-9649 [Electronic] England |
PMID | 26247846
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Copyright | Copyright © 2015 Elsevier B.V. All rights reserved. |
Chemical References |
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Topics |
- Aging
(pathology, physiology)
- Apoptosis
- Estradiol
(metabolism)
- Humans
- Sarcopenia
(metabolism, pathology)
- Satellite Cells, Skeletal Muscle
(metabolism, pathology)
- Testosterone
(metabolism)
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