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肿瘤坏死因子(Tumor necrosis factor,TNF)是一种能使肿瘤发生坏死的物质,主要由内毒素激活单核/巨噬细胞产生,是启动抗菌炎症反应的关键细胞因子[1]。长期以来,动物及人体实验均发现,慢性感染、肌萎缩、恶病质和杜氏肌营养不良等消耗性疾病以及正常的衰老进程中,血液TNF-α水平和/或骨骼肌TNF-α表达增多并伴随骨骼肌丢失[2-4],因此,传统观点认为TNF-α是一个负性调节因子,但近年来有研究发现,肿瘤坏死因子中的TNF-α能通过p38MAPK和NF-κB信号途径影响肌肉再生过程,对骨骼肌的损伤和修复可能起到重要的调节作用。
Tumor necrosis factor (TNF), a substance that causes tumor necrosis, is produced mainly by endotoxin-activated monocytes / macrophages and is a key cytokine that initiates an anti-bacterial inflammatory response [1]. For a long time, animal and human experiments have found that blood TNF-α levels and / or skeletal muscle TNF-α expression are increased along with chronic diseases such as chronic infection, muscle wasting, cachexia and Duchenne muscular dystrophy and normal aging process Therefore, the traditional view that TNF-α is a negative regulator, but in recent years, studies have found that tumor necrosis factor TNF-α through the p38MAPK and NF-κB signaling pathway affect the muscles Regeneration process, the damage and repair of skeletal muscle may play an important regulatory role.