Emerging Strategies Targeting Catabolic Muscle Stress Relief
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 prove...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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MDPI AG
2020-06-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/21/13/4681 |
| _version_ | 1797563674479558656 |
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| author | Mattia Scalabrin Volker Adams Siegfried Labeit T. Scott Bowen |
| author_facet | Mattia Scalabrin Volker Adams Siegfried Labeit T. Scott Bowen |
| author_sort | Mattia Scalabrin |
| collection | DOAJ |
| description | 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 (NFκB) inhibitors, myostatin antibodies, β<sub>2</sub> adrenergic agonists, and small-molecules interfering with MuRF1, which all emerge as a novel in vivo treatment strategies for muscle wasting. |
| first_indexed | 2024-03-10T18:46:49Z |
| format | Article |
| id | doaj.art-c6b198b9cdcc4866bc1a2373b2323040 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-10T18:46:49Z |
| publishDate | 2020-06-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-c6b198b9cdcc4866bc1a2373b23230402023-11-20T05:29:38ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672020-06-012113468110.3390/ijms21134681Emerging Strategies Targeting Catabolic Muscle Stress ReliefMattia Scalabrin0Volker Adams1Siegfried Labeit2T. Scott Bowen3School of Biomedical Sciences, University of Leeds, Leeds LS2 9JT, UKDepartment of Experimental and Molecular Cardiology, TU Dresden, Heart Center Dresden, 01307 Dresden, GermanyMedical Faculty Mannheim, University of Heidelberg, 68167 Mannheim, GermanySchool of Biomedical Sciences, University of Leeds, Leeds LS2 9JT, UKSkeletal 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 (NFκB) inhibitors, myostatin antibodies, β<sub>2</sub> adrenergic agonists, and small-molecules interfering with MuRF1, which all emerge as a novel in vivo treatment strategies for muscle wasting.https://www.mdpi.com/1422-0067/21/13/4681atrophydiaphragmdisusemitochondriaMuRF1MuRF2 |
| spellingShingle | Mattia Scalabrin Volker Adams Siegfried Labeit T. Scott Bowen Emerging Strategies Targeting Catabolic Muscle Stress Relief International Journal of Molecular Sciences atrophy diaphragm disuse mitochondria MuRF1 MuRF2 |
| title | Emerging Strategies Targeting Catabolic Muscle Stress Relief |
| title_full | Emerging Strategies Targeting Catabolic Muscle Stress Relief |
| title_fullStr | Emerging Strategies Targeting Catabolic Muscle Stress Relief |
| title_full_unstemmed | Emerging Strategies Targeting Catabolic Muscle Stress Relief |
| title_short | Emerging Strategies Targeting Catabolic Muscle Stress Relief |
| title_sort | emerging strategies targeting catabolic muscle stress relief |
| topic | atrophy diaphragm disuse mitochondria MuRF1 MuRF2 |
| url | https://www.mdpi.com/1422-0067/21/13/4681 |
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