Cancer Cachexia: Mediators, Signaling, and Metabolic Pathways

被引：892

作者：

Fearon, Kenneth C. H. ^{[1
]}

Glass, David J. ^{[2
]}

Guttridge, Denis C. ^{[3
]}

机构：

[1] Univ Edinburgh, Royal Infirm, Sch Clin Sci & Community Hlth, Edinburgh EH16 4SA, Midlothian, Scotland

[2] Novartis Inst Biomed Res, Cambridge, MA 02139 USA

[3] Ohio State Univ, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA

来源：

CELL METABOLISM | 2012年 / 16卷 / 02期

关键词：

SKELETAL-MUSCLE ATROPHY; TUMOR-NECROSIS-FACTOR; ACUTE-PHASE RESPONSE; UBIQUITIN LIGASE ATROGIN1/MAFBX; ADIPOSE TRIGLYCERIDE LIPASE; PROTEOLYSIS INDUCING FACTOR; FOXO TRANSCRIPTION FACTORS; SYNTHASE KINASE 3-BETA; MESSENGER-RNA LEVELS; KAPPA-B ACTIVATION;

D O I：

10.1016/j.cmet.2012.06.011

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

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.

引用

页码：153 / 166

页数：14

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