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首页> 外文期刊>Current opinion in clinical nutrition and metabolic care >Skeletal muscle cytokines: regulation by pathogen-associated molecules and catabolic hormones.
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Skeletal muscle cytokines: regulation by pathogen-associated molecules and catabolic hormones.

机译：骨骼肌细胞因子：由病原体相关分子和分解代谢激素调节。

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PURPOSE OF REVIEW: This review will update clinicians and basic scientists who study the molecular mechanisms of muscle wasting associated with infection, trauma, cancer cachexia, and AIDS. A special emphasis is placed on recent studies that examine the interaction of insulin-like growth factor 1 and proinflammatory cytokines as positive and negative regulators of muscle mass. RECENT FINDINGS: Potential mediators of the wasting syndromes include catabolic hormones, such as glucocorticoids, as well as the inflammatory cytokines tumour necrosis factor, IL-1, and IL-6. Cytokines may function either systemically or locally within muscle per se. Lipopolysaccharide and other pathogen-associated molecules stimulate cytokine expression in muscle. The failure to clear pathogen-associated molecules or the introduction of muscle damage may initiate a protracted activation of enzymes and transcription factors that orchestrate a genetic programme that ultimately produces muscle wasting. SUMMARY: This review highlights recent advances in our understanding of the expression of the afferent and efferent limbs of the innate immune system in skeletal muscle. A special emphasis is placed on the recognition of pathogen-associated molecules by skeletal muscle cells and how these molecules regulate the expression of inflammatory cytokines and other muscle genes to result in muscle wasting, and when sustained, the erosion of lean body mass.
机译：审查目的：这项审查将更新研究与感染，创伤，癌症恶病质和艾滋病相关的肌肉消瘦的分子机制的临床医生和基础科学家。特别强调的是最近的研究，这些研究检查了胰岛素样生长因子1和促炎细胞因子作为肌肉质量的正负调节剂之间的相互作用。最近的发现：消瘦综合症的潜在介质包括糖代谢激素等分解代谢激素，以及炎性细胞因子肿瘤坏死因子IL-1和IL-6。细胞因子本身可以在肌肉内全身或局部起作用。脂多糖和其他病原体相关分子刺激肌肉中细胞因子的表达。无法清除病原体相关分子或引入肌肉损伤可能会导致酶和转录因子的长期激活，从而导致最终导致肌肉浪费的基因程序的编排。摘要：这篇综述突出了我们对骨骼肌先天免疫系统传入和传出肢体表达的理解的最新进展。特别强调骨骼肌细胞对病原体相关分子的识别，以及这些分子如何调节炎性细胞因子和其他肌肉基因的表达，从而导致肌肉消瘦，以及持续时对瘦体重的侵蚀。

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