In:
American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 323, No. 4 ( 2022-10-01), p. C974-C989
Abstract:
Locomotor skeletal muscle dysfunction is a relevant comorbidity of chronic obstructive pulmonary disease (COPD) and is strongly associated with worse clinical outcomes including higher mortality. Over the last decades, a large body of literature helped characterize the process, defining the disruptive muscle phenotype caused by COPD that involves reduction in muscle mass, force-generation capacity, fatigue-tolerance, and regenerative potential following injury. A major limitation in the field has been the scarcity of well-calibrated animal models to conduct mechanistic research based on loss- and gain-of-function studies. This article provides an overall description of the process, the tools available to mechanistically investigate it, and the potential role of mitochondrially driven metabolic signals on the regulation muscle regeneration after injury in COPD. Finally, a description of future avenues to further expand on the area is proposed based on very recent evidence involving mitochondrial metabolic cues affecting myogenesis.
Type of Medium:
Online Resource
ISSN:
0363-6143
,
1522-1563
DOI:
10.1152/ajpcell.00292.2022
Language:
English
Publisher:
American Physiological Society
Publication Date:
2022
detail.hit.zdb_id:
1477334-X
SSG:
12
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