骨骼肌
肌发生
心肌细胞
肿瘤坏死因子α
旁分泌信号
自分泌信号
调解人
医学
内分泌学
细胞因子
内科学
分解代谢
新陈代谢
受体
作者
Yiping Li,Michael B. Reid
出处
期刊:Current Opinion in Rheumatology
[Ovid Technologies (Wolters Kluwer)]
日期:2001-11-01
卷期号:13 (6): 483-487
被引量:112
标识
DOI:10.1097/00002281-200111000-00005
摘要
Over the past year, considerable progress has been made in our understanding of biologic actions by which tumor necrosis factor-α (TNF-α) may influence skeletal muscle metabolism. Reports published during this period highlighted three general actions with metabolic consequences: accelerated catabolism (protein loss, insulin resistance), contractile dysfunction, and disruption of myogenesis. Recent research also indicates that skeletal muscle myocytes synthesize TNF-α and that the cytokine functions as an endogenous mediator of muscle adaptation via autocrine/paracrine effects. These advances demonstrate the fundamental importance of TNF-α effects on skeletal muscle myocytes and provide a focus for future studies of intracellular mechanism.
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