The dependency of autophagy and ubiquitin proteasome system during skeletal muscle atrophy.
Autophagy
Mitophagy
Molecular mechanism
Skeletal muscle atrophy
The ubiquitin-proteasome system
Journal
Biophysical reviews
ISSN: 1867-2450
Titre abrégé: Biophys Rev
Pays: Germany
ID NLM: 101498573
Informations de publication
Date de publication:
Apr 2021
Apr 2021
Historique:
received:
29
10
2020
accepted:
24
02
2021
entrez:
30
4
2021
pubmed:
1
5
2021
medline:
1
5
2021
Statut:
epublish
Résumé
Among the four proteolytic systems in the cell, autophagy and the ubiquitin-proteasome system (UPS) are the main proteolytic events that allow for the removal of cell debris and proteins to maintain cellular homeostasis. Previous studies have revealed that these systems perform their functions independently of each other. However, recent studies indicate the existence of regulatory interactions between these proteolytic systems via ubiquitinated tags and a reciprocal regulation mechanism with several crosstalk points. UPS plays an important role in the elimination of short-lived/soluble misfolded proteins, whereas autophagy eliminates defective organelles and persistent insoluble protein aggregates. Both of these systems seem to act independently; however, disruption of one pathway affects the activity of the other pathway and contributes to different pathological conditions. This review summarizes the recent findings on direct and indirect dependencies of autophagy and UPS and their execution at the molecular level along with the important drug targets in skeletal muscle atrophy.
Identifiants
pubmed: 33927785
doi: 10.1007/s12551-021-00789-7
pii: 789
pmc: PMC8046863
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
203-219Informations de copyright
© International Union for Pure and Applied Biophysics (IUPAB) and Springer-Verlag GmbH Germany, part of Springer Nature 2021.
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