Emerging Strategies Targeting Catabolic Muscle Stress Relief.
MuRF1
MuRF2
atrophy
diaphragm
disuse
mitochondria
skeletal muscle
ubiquitin
wasting
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
30 Jun 2020
30 Jun 2020
Historique:
received:
04
06
2020
revised:
26
06
2020
accepted:
29
06
2020
entrez:
8
7
2020
pubmed:
8
7
2020
medline:
27
2
2021
Statut:
epublish
Résumé
Skeletal muscle wasting represents a common trait in many conditions, including aging, cancer, heart failure, immobilization, and critical illness. Loss of muscle mass leads to impaired functional mobility and severely impedes the quality of life. At present, exercise training remains the only proven treatment for muscle atrophy, yet many patients are too ill, frail, bedridden, or neurologically impaired to perform physical exertion. The development of novel therapeutic strategies that can be applied to an in vivo context and attenuate secondary myopathies represents an unmet medical need. This review discusses recent progress in understanding the molecular pathways involved in regulating skeletal muscle wasting with a focus on pro-catabolic factors, in particular, the ubiquitin-proteasome system and its activating muscle-specific E3 ligase RING-finger protein 1 (MuRF1). Mechanistic progress has provided the opportunity to design experimental therapeutic concepts that may affect the ubiquitin-proteasome system and prevent subsequent muscle wasting, with novel advances made in regards to nutritional supplements, nuclear factor kappa-light-chain-enhancer of activated B cells (NFB) inhibitors, myostatin antibodies, β
Identifiants
pubmed: 32630118
pii: ijms21134681
doi: 10.3390/ijms21134681
pmc: PMC7369951
pii:
doi:
Substances chimiques
Muscle Proteins
0
Tripartite Motif Proteins
0
Ubiquitin
0
TRIM63 protein, human
EC 2.3.2.27
Ubiquitin-Protein Ligases
EC 2.3.2.27
Proteasome Endopeptidase Complex
EC 3.4.25.1
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Medical Research Council
ID : MR/S025472/1
Pays : United Kingdom
Organisme : Heart Research UK
ID : TRP 16/19
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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