期刊
JOURNAL OF CACHEXIA SARCOPENIA AND MUSCLE
卷 3, 期 3, 页码 163-179出版社
WILEY
DOI: 10.1007/s13539-012-0074-6
关键词
Skeletal muscle atrophy; Cachexia; Proteasome; Autophagy; Apoptosis; Therapy
资金
- Fund for Scientific Research (FWO)-Flanders (Belgium)
- University of Antwerp
- Associazione Amici per il Cuore-ONLUS, Chiari (Brescia)-Italy
- University of Brescia research fund
- Associazione Italiana per la Ricerca sul Cancro Funding Source: Custom
Skeletal muscle atrophy is defined as a decrease in muscle mass and it occurs when protein degradation exceeds protein synthesis. Potential triggers of muscle wasting are long-term immobilization, malnutrition, severe burns, aging as well as various serious and often chronic diseases, such as chronic heart failure, obstructive lung disease, renal failure, AIDS, sepsis, immune disorders, cancer, and dystrophies. Interestingly, a cooperation between several pathophysiological factors, including inappropriately adapted anabolic (e.g., growth hormone, insulin-like growth factor 1) and catabolic proteins (e.g., tumor necrosis factor alpha, myostatin), may tip the balance towards muscle-specific protein degradation through activation of the proteasomal and autophagic systems or the apoptotic pathway. Based on the current literature, we present an overview of the molecular and cellular mechanisms that contribute to muscle wasting. We also focus on the multifacetted therapeutic approach that is currently employed to prevent the development of muscle wasting and to counteract its progression. This approach includes adequate nutritional support, implementation of exercise training, and possible pharmacological compounds.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据