The role of E3 ubiquitin-ligases MuRF-1 and MAFbx in loss of skeletal muscle mass
| Autor: | Oren Rom, Abraham Z. Reznick |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Proteasome Endopeptidase Complex medicine.medical_specialty Ubiquitin-Protein Ligases Muscle Proteins Protein degradation Biochemistry Tripartite Motif Proteins Mice 03 medical and health sciences 0302 clinical medicine Ubiquitin Physiology (medical) Internal medicine Diabetes mellitus medicine Animals Humans Disease Muscle Skeletal Exercise Life Style Ubiquitins Wasting SKP Cullin F-Box Protein Ligases biology business.industry Skeletal muscle medicine.disease Muscle atrophy 030104 developmental biology Endocrinology medicine.anatomical_structure Proteasome Sarcopenia biology.protein Atrophy medicine.symptom business 030217 neurology & neurosurgery |
| Zdroj: | Free Radical Biology and Medicine. 98:218-230 |
| ISSN: | 0891-5849 |
| DOI: | 10.1016/j.freeradbiomed.2015.12.031 |
| Popis: | The ubiquitin-proteasome system (UPS) is the main regulatory mechanism of protein degradation in skeletal muscle. The ubiquitin-ligase enzymes (E3s) have a central role in determining the selectivity and specificity of the UPS. Since their identification in 2001, the muscle specific E3s, muscle RING finger-1 (MuRF-1) and muscle atrophy F-box (MAFbx), have been shown to be implicated in the regulation of skeletal muscle atrophy in various pathological and physiological conditions. This review aims to explore the involvement of MuRF-1 and MAFbx in catabolism of skeletal muscle during various pathologies, such as cancer cachexia, sarcopenia of aging, chronic kidney disease (CKD), diabetes, and chronic obstructive pulmonary disease (COPD). In addition, the effects of various lifestyle and modifiable factors (e.g. nutrition, exercise, cigarette smoking, and alcohol) on MuRF-1 and MAFbx regulation will be discussed. Finally, evidence of potential strategies to protect against skeletal muscle wasting through inhibition of MuRF-1 and MAFbx expression will be explored. |
| Databáze: | OpenAIRE |
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