Argilés Josep M, Busquets Silvia, Stemmler Britta, López-Soriano Francisco J
Cancer Research Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain; Institut de Biomedicina de la Universitat de Barcelona, Barcelona, Spain.
Cancer Research Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain; Institut de Biomedicina de la Universitat de Barcelona, Barcelona, Spain.
Curr Opin Pharmacol. 2015 Jun;22:100-6. doi: 10.1016/j.coph.2015.04.003. Epub 2015 May 14.
Cachexia is a multi-organ syndrome associated with cancer and other chronic diseases, characterized by body weight loss, muscle and adipose tissue wasting and inflammation, being often associated with anorexia. Skeletal muscle tissue represents more than 40% of body weight and seems to be one of the main tissues involved in the wasting that occurs during cachexia. Sarcopenia is a degenerative loss of skeletal muscle mass, quality, and strength associated with healthy ageing. The molecular mechanisms behind cachexia and sarcopenia share some common trends. Muscle wasting is the result of a combination of an imbalance between synthetic and degradative protein pathways together with increased myocyte apoptosis and decreased regenerative capacity. Oxidative pathways are also altered in skeletal muscle during muscle wasting and this seems to be a consequence of mitochondrial abnormalities that include altered morphology and function, decreased ATP synthesis and uncoupling. The aim of the present review is to analyse common molecular pathways between cachexia and sarcopenia in order to put forward potential targets for intervention.
恶病质是一种与癌症和其他慢性疾病相关的多器官综合征，其特征为体重减轻、肌肉和脂肪组织消耗以及炎症，常伴有厌食。骨骼肌组织占体重的40%以上，似乎是恶病质期间发生消耗的主要组织之一。肌肉减少症是与健康衰老相关的骨骼肌质量、质量和力量的退行性丧失。恶病质和肌肉减少症背后的分子机制有一些共同趋势。肌肉消耗是合成和降解蛋白途径失衡、肌细胞凋亡增加以及再生能力下降共同作用的结果。在肌肉消耗期间，骨骼肌中的氧化途径也会改变，这似乎是线粒体异常的结果，线粒体异常包括形态和功能改变、ATP合成减少和解偶联。本综述的目的是分析恶病质和肌肉减少症之间的共同分子途径，以便提出潜在的干预靶点。
