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Mitochondrion. 2020 Jan;50:63-70. doi: 10.1016/j.mito.2019.10.007. Epub 2019 Oct 24.

Extracellular matrix/mitochondria pathway: A novel potential target for sarcopenia.

Author information

1
CREMI, CHU de Québec Research Center, Quebec G1V 4G2, Canada; Department of Molecular Medicine, Faculty of Medicine, Laval University, Quebec G1V 4G2, Canada.
2
CREMI, CHU de Québec Research Center, Quebec G1V 4G2, Canada.
3
CREMI, CHU de Québec Research Center, Quebec G1V 4G2, Canada; Department of Molecular Medicine, Faculty of Medicine, Laval University, Quebec G1V 4G2, Canada. Electronic address: jonny.St-Amand@crchudequebec.ulaval.ca.

Abstract

Sarcopenia is a geriatric syndrome characterized by a progressive and generalized loss of muscle mass, strength, and endurance. Although the mitochondrial hypothesis of sarcopenia has been proposed, it remains a highly debated topic. The age-related declines in skeletal muscle regenerative capacity have been attributed to the changes in the extracellular matrix (ECM) composition. Therefore, mitochondrial deterioration in the muscle may be implicated in the sarcopenic process, and a possible link between ECM remodeling and mitochondrial dysfunction may be suggested. While exercise training improves elderly muscle function, the contradictory results obtained from different studies, the lack of a well-defined training program as well as age-related falls may raise questions regarding the overall benefits of this interventional strategy for sarcopenic elderly who have limited ability to perform physical exercise. Thus, it remains important to be able to offer less cumbersome but equally effective alternatives such as pharmacological approaches to help elderly patients. In this review, we discuss the involvement of mitochondrial dysfunction as well as the ECM remodeling in sarcopenia, and we suggest that the future of sarcopenia drug development may be targeting ECM/mitochondria pathway.

KEYWORDS:

ECM remodeling; Mitochondria dysfunction; New pathway; Sarcopenia

PMID:
31669412
DOI:
10.1016/j.mito.2019.10.007

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