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癌症恶病质:介质、信号和代谢途径。

Cancer cachexia: mediators, signaling, and metabolic pathways.

机构信息

Clinical Surgery, School of Clinical Sciences and Community Health, University of Edinburgh, Royal Infirmary, Edinburgh EH16 4SA, UK.

出版信息

Cell Metab. 2012 Aug 8;16(2):153-66. doi: 10.1016/j.cmet.2012.06.011. Epub 2012 Jul 12.

DOI:10.1016/j.cmet.2012.06.011
PMID:22795476
Abstract

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.

摘要

癌症恶病质的特征是体重显著下降,主要是由于脂肪组织和骨骼肌的丧失。恶病质导致癌症治疗耐受性降低,生活质量和寿命缩短,仍然是未满足的医疗需求。治疗进展受到阻碍,部分原因是在模型系统内和之间,以及在临床综合征中,介质、信号和代谢途径的明显异质性。最近在理解骨骼肌萎缩/肥大的保守分子机制方面取得的进展,为规避上游介质的变异性和冗余性提供了下游平台,最终可能转化为新的靶向治疗。

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