期刊文献+

Muscle mitochondria and oxidative metabolism as targets against cancer cachexia

原文传递
导出
摘要 Cancer cachexia is a debilitating syndrome mainly characterized by muscle and fat wasting, leading to the progressive loss of body weight and complicating the management of cancer patient. In particular, the loss of muscle weight is a negative prognostic factor, being associated with chemotherapy toxicity and reduced survival. Increased inflammation and protein dysmetabolism are some of the impairments that lead to muscle wasting in cancer patients. Together with these alterations, tumor growth and chemotherapy administration may affect mitochondrial function, impinging on the muscle energy metabolism. Indeed, therapeutic approaches poised to correct both hypercatabolism and mitochondrial alterations could be effective in preventing cancer-induced muscle wasting. Among the non-pharmacological approaches, exercise training is one of the best modulator of muscle physiology able to impinge on both protein and energy metabolism. However, the wasting phenotype that characterizes cancer patients could be not compatible with physical training, prompting the development of different strategies to improve muscle metabolism. The aim of this mini-review is to discuss both the beneficial effects and the limitations of exercise training in cancer cachexia and the adoption of drugs able to modulate exercise-induced pathways.
出处 《Journal of Cancer Metastasis and Treatment》 2019年第8期3-11,共9页 癌症转移与治疗(英文版)
  • 相关文献

参考文献1

二级参考文献65

  • 1Dillon LM,Rebelo AP,Moraes CT. The role of PG C-1 coactivators in aging skeletal muscle and heart[J].IUBMB Life,2012.231-241.
  • 2Wallace DC. A mitoohondrial paradigm of metabolic and degenerative diseases,aging,and cancer:a dawn for evolutionary medicine[J].Annual Review of Genetics,2005.359-407.
  • 3Handschin C,Spiegelman BM. The role of exercise and PGC1α in inflammation and chronic disease[J].Nature,2008,(7203):463-469.
  • 4Finkel T,Holbrook NJ. Oxidants,oxidative stress and the biology of ageing[J].Nature,2000.239-247.
  • 5Ryan MT,Hoogenraad NJ. Mitochondrial-nuclear communications[J].Annual Review of Biochemistry,2007.701-722.
  • 6Hoppeler H,Fluck M. Plasticity of skeletal muscle mitoohondria:structure and function[J].Medicine and Science in Sports and Exercise,2003.95-104.
  • 7Wu Z,Puigserver P,Andersson U,Zhang C,Adelmant G.Mootha V. Mechanisms controlling mitochondrial biogenesis and function through the thermogenic coactivator PGC-1[J].Cell,1999.115-124.
  • 8Wenz T,Rossi SG,Rotundo RL,Spiegelman BM Moraes CT. Increased muscle PGC-1α expression protects from sarcopenia and metabolic disease during aging[J].Proceedings of the National Academy of Sciences(USA),2009.20405-20410.
  • 9Puigserver P,Wu Z,Park CW,Graves R,Wright M,Spiegelman BM. A cold-inducible coactivator of nuclear receptors linked to adaptive thermogenesis[J].Cell,1998,(6):829-839.doi:10.1016/S0092-8674(00)81410-5.
  • 10Lin J,Wu H,Tarr PT,Zhang CY Wu Z Boss O. Transcriptional coactivator PGC-1α drives the formation of slow-twitch muscle fibres[J].Nature,2002.797-801.

共引文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部