恶病质
骨骼肌
脂肪组织
癌症
生物
肌肉萎缩
肌萎缩
癌症研究
肌肉肥大
生物信息学
信号转导
萎缩
医学
内分泌学
内科学
细胞生物学
作者
Kenneth C.H. Fearon,David J. Glass,Denis C. Guttridge
出处
期刊:Cell Metabolism
[Cell Press]
日期:2012-07-17
卷期号:16 (2): 153-166
被引量:1208
标识
DOI:10.1016/j.cmet.2012.06.011
摘要
Cancer cachexia is characterized by a significant reduction in body weight resulting predominantly from loss of adipose tissue and skeletal muscle. Cachexia causes reduced cancer treatment tolerance and reduced quality and length of life, and remains an unmet medical need. Therapeutic progress has been impeded, in part, by the marked heterogeneity of mediators, signaling, and metabolic pathways both within and between model systems and the clinical syndrome. Recent progress in understanding conserved, molecular mechanisms of skeletal muscle atrophy/hypertrophy has provided a downstream platform for circumventing the variations and redundancy in upstream mediators and may ultimately translate into new targeted therapies.
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