Báo cáo y học: " α Tumor necrosis factor-α and muscle wasting: a cellular perspective"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài:" α Tumor necrosis factor-α and muscle wasting: a cellular perspective. | Available online http content 2 5 269 Commentary Tumor necrosis factor-a and muscle wasting a cellular perspective Michael B Reid and Yi-Ping Li Pulmonary Section Baylor College of Medicine Houston Texas USA Correspondence Michael B. Reid Pulmonary Section Suite 520B Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA. Tel 713-798-7224 fax 1 713 798 3619 e-mail reid@ o 3 I Received 30 April 2001 Revisions requested 15 May 2001 Revisions received 2 June 2001 Accepted 12 June 2001 Published 12 July 2001 Respir Res 2001 2 269-272 2001 BioMed Central Ltd Print ISSN 1465-9921 Online ISSN 1465-993X Abstract Tumor necrosis factor-a TNF-a is a polypeptide cytokine that has been associated with muscle wasting and weakness in inflammatory disease. Despite its potential importance in muscle pathology the direct effects of TNF-a on skeletal muscle have remained undefined until recently. Studies of cultured muscle cells indicate that TNF-a disrupts the differentiation process and can promote catabolism in mature cells. The latter response appears to be mediated by reactive oxygen species and nuclear factor-KB which upregulate ubiquitin proteasome activity. This commentary outlines our current understanding of TNF-a effects on skeletal muscle and the mechanism of TNF-a action. Keywords antioxidants cachexia cytokines free radicals skeletal muscle Introduction TNF-a is a polypeptide cytokine that promotes antitumor and immune responses 1 . TNF-a has long been associated with muscle pathology and was originally designated cachectin in recognition of its catabolic action. Experimental animals lose muscle mass when treated with TNF-a 2 3 or exposed to interventions that elevate endogenous TNF-a . sepsis or tumor implantation . In humans muscle catabolism has been attributed to TNF-a in inflammatory diseases that include cancer 4 congestive heart failure 5 AIDS 6 and chronic obstructive pulmonary disease COPD 7 . In the latter case

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