自噬
医学
心肌细胞
药品
肌肉萎缩
毒性
肌病
药理学
线粒体肌病
肌炎
细胞凋亡
萎缩
生物信息学
内科学
生物
生物化学
线粒体DNA
基因
作者
Jonathan D. G. Jones,Hannah Kirsch,Robert L. Wortmann,Michael H. Pillinger
出处
期刊:Current Opinion in Rheumatology
[Ovid Technologies (Wolters Kluwer)]
日期:2014-09-05
卷期号:26 (6): 697-703
被引量:22
标识
DOI:10.1097/bor.0000000000000108
摘要
Purpose of review Clinically identified myopathies are frequently a consequence of medication toxicities. However, recognizing drug-induced myopathies is sometimes difficult. Developing a greater understanding of the underlying mechanisms of drug-induced muscle toxicity will promote enhanced awareness and recognition, and improved management of these syndromes. Recent findings The adverse impact of certain drugs on muscle metabolism, muscle cell atrophy, and myocyte apoptosis is increasingly clear. Glucocorticoids impair glucose handling and directly promote protein catabolism. Statins impair mitochondrial function and alter intracellular signaling proteins, which can lead to myocyte apoptosis. Alternatively, statins can induce an autoimmune necrotizing myositis. Several medications impair autophagy, thus limiting access to the needed glycogen stores. Summary This review provides an overview of the main underlying mechanisms of drug-induced myopathies. These myopathies will most often be related to a drug's ability to alter metabolism and protein balance, induce necrosis, or impair autophagy.
科研通智能强力驱动
Strongly Powered by AbleSci AI