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Tumor necrosis factor-alpha and muscle wasting: a cellular perspective
1Pulmonary Section, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA. reid@bcm.tmc.edu
Respiratory Research
|November 1, 2001
Summary
Tumor necrosis factor-alpha (TNF-alpha) disrupts skeletal muscle differentiation and promotes catabolism in mature cells. This cytokine
Area of Science:
- Biochemistry
- Cell Biology
- Immunology
Background:
- Tumor necrosis factor-alpha (TNF-alpha) is linked to muscle wasting in inflammatory conditions.
- Direct effects of TNF-alpha on skeletal muscle were previously unclear.
Purpose of the Study:
- To outline the current understanding of TNF-alpha's effects on skeletal muscle.
- To elucidate the mechanisms of TNF-alpha action in muscle cells.
Main Methods:
- Studies utilized cultured muscle cells.
- Analysis focused on cellular differentiation and catabolism.
Main Results:
- TNF-alpha was found to disrupt muscle cell differentiation.
- Mature muscle cells treated with TNF-alpha exhibited increased catabolism.
- Reactive oxygen species and nuclear factor-kappaB mediate TNF-alpha-induced catabolism via ubiquitin/proteasome activity.
Conclusions:
- TNF-alpha directly impacts skeletal muscle by inhibiting differentiation and promoting breakdown.
- The ubiquitin/proteasome pathway, regulated by reactive oxygen species and NF-kappaB, is a key mediator of TNF-alpha's catabolic effects.