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Ubiquitin ligases in longevity and aging skeletal muscle
Journal article   Open access   Peer reviewed

Ubiquitin ligases in longevity and aging skeletal muscle

David C. Hughes, Leslie M. Baehr, David S. Waddell, Adam Sharples and Sue C Bodine
International journal of molecular sciences, Vol.23(14), 7602
07/09/2022
DOI: 10.3390/ijms23147602
PMCID: PMC9315556
PMID: 35886949
url
https://doi.org/10.3390/ijms23147602View
Published (Version of record) Open Access

Abstract

The development and prevalence of diseases associated with aging presents a global health burden on society. One hallmark of aging is the loss of proteostasis which is caused in part by alterations to the ubiquitin–proteasome system (UPS) and lysosome–autophagy system leading to impaired function and maintenance of mass in tissues such as skeletal muscle. In the instance of skeletal muscle, the impairment of function occurs early in the aging process and is dependent on proteostatic mechanisms. The UPS plays a pivotal role in degradation of misfolded and aggregated proteins. For the purpose of this review, we will discuss the role of the UPS system in the context of age-related loss of muscle mass and function. We highlight the significant role that E3 ubiquitin ligases play in the turnover of key components (e.g., mitochondria and neuromuscular junction) essential to skeletal muscle function and the influence of aging. In addition, we will briefly discuss the contribution of the UPS system to lifespan. By understanding the UPS system as part of the proteostasis network in age-related diseases and disorders such as sarcopenia, new discoveries can be made and new interventions can be developed which will preserve muscle function and maintain quality of life with advancing age. publishedVersion Institutt for fysisk prestasjonsevne / Department of Physical Performance
 healthspan protein degradation proteostasis sarcopenia E3 ubiquitin ligase

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