分解代谢
促炎细胞因子
蛋白质降解
蛋白酶体
蛋白质分解代谢
蛋白质水解
骨骼肌
肌肉萎缩
泛素
蛋白质周转
肌肉蛋白
内分泌学
刺激
内科学
糖皮质激素
化学
胞浆
合成代谢
炎症
蛋白质生物合成
生物
生物化学
医学
新陈代谢
酶
氨基酸
基因
出处
期刊:Current Opinion in Clinical Nutrition and Metabolic Care
[Ovid Technologies (Wolters Kluwer)]
日期:1999-05-01
卷期号:2 (3): 201-205
被引量:267
标识
DOI:10.1097/00075197-199905000-00002
摘要
Glucocorticoids inhibit protein synthesis and stimulate protein degradation in skeletal muscle and are an important factor in the development of muscle atrophy in various catabolic conditions. Glucocorticoid-stimulated muscle protein breakdown is primarily caused by ubiquitin-proteasome-dependent proteolysis although calcium-dependent protein degradation may also be involved. In certain catabolic conditions, including sepsis, an interaction between glucocorticoids and proinflammatory cytokines is important for the stimulation of muscle protein breakdown.
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