Cytokine Signaling in Skeletal Muscle Wasting. (May 2016)
- Record Type:
- Journal Article
- Title:
- Cytokine Signaling in Skeletal Muscle Wasting. (May 2016)
- Main Title:
- Cytokine Signaling in Skeletal Muscle Wasting
- Authors:
- Zhou, Jin
Liu, Bin
Liang, Chun
Li, Yangxin
Song, Yao-Hua - Abstract:
- Abstract : Skeletal muscle wasting occurs in a variety of diseases including diabetes, cancer, Crohn's disease, chronic obstructive pulmonary disease (COPD), disuse, and denervation. Tumor necrosis factor α (TNF-α) is involved in mediating the wasting effect. To date, a causal relationship between TNF-α signaling and muscle wasting has been established in animal models. However, results from clinical trials are conflicting. This is partly due to the fact that other factors such as TNF-like weak inducer of apoptosis (TWEAK) and interleukin 6 (IL-6) are also involved in skeletal muscle wasting. Because muscle wasting is often associated with physical inactivity and reduced food intake, therapeutic interventions will be most effective when multiple approaches are used in conjunction with nutritional support and exercise. Trends: Muscle wasting is the result of an imbalance between anabolic and catabolic metabolism due to inflammation, physical inactivity, and inadequate nutrition. TNF-α, IL-6, and TWEAK shift the metabolism balance toward a catabolic process. However, current therapies such as neutralizing antibodies/decoy receptors against TNF-α, IL-6, and nonsteroidal anti-inflammatory drugs had limited success when used alone. These specific therapies will be more successful when combined with nutritional support, appetite stimulators, and exercise, because combinatorial approaches will not only inhibit protein degradation but also promote protein synthesis. Clinical trialsAbstract : Skeletal muscle wasting occurs in a variety of diseases including diabetes, cancer, Crohn's disease, chronic obstructive pulmonary disease (COPD), disuse, and denervation. Tumor necrosis factor α (TNF-α) is involved in mediating the wasting effect. To date, a causal relationship between TNF-α signaling and muscle wasting has been established in animal models. However, results from clinical trials are conflicting. This is partly due to the fact that other factors such as TNF-like weak inducer of apoptosis (TWEAK) and interleukin 6 (IL-6) are also involved in skeletal muscle wasting. Because muscle wasting is often associated with physical inactivity and reduced food intake, therapeutic interventions will be most effective when multiple approaches are used in conjunction with nutritional support and exercise. Trends: Muscle wasting is the result of an imbalance between anabolic and catabolic metabolism due to inflammation, physical inactivity, and inadequate nutrition. TNF-α, IL-6, and TWEAK shift the metabolism balance toward a catabolic process. However, current therapies such as neutralizing antibodies/decoy receptors against TNF-α, IL-6, and nonsteroidal anti-inflammatory drugs had limited success when used alone. These specific therapies will be more successful when combined with nutritional support, appetite stimulators, and exercise, because combinatorial approaches will not only inhibit protein degradation but also promote protein synthesis. Clinical trials are warranted and will yield more conclusive results by measuring cytokine levels from each patient prior to treatment. … (more)
- Is Part Of:
- Trends in endocrinology and metabolism. Volume 27:Number 5(2016)
- Journal:
- Trends in endocrinology and metabolism
- Issue:
- Volume 27:Number 5(2016)
- Issue Display:
- Volume 27, Issue 5 (2016)
- Year:
- 2016
- Volume:
- 27
- Issue:
- 5
- Issue Sort Value:
- 2016-0027-0005-0000
- Page Start:
- 335
- Page End:
- 347
- Publication Date:
- 2016-05
- Subjects:
- TNF-α -- muscle wasting -- TWEAK -- TRAF6
Endocrinology -- Periodicals
Metabolism -- Periodicals
Metabolism
616.4 - Journal URLs:
- http://www.elsevier.com/journals ↗
http://www.sciencedirect.com/science/journal/10432760 ↗ - DOI:
- 10.1016/j.tem.2016.03.002 ↗
- Languages:
- English
- ISSNs:
- 1043-2760
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 9049.590500
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 8827.xml