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自噬对炎症小体的调节。

Regulation of inflammasomes by autophagy.

机构信息

Department of Inflammation Biology, Institute for Enzyme Research, Tokushima University, Tokushima, Japan.

Laboratory of Host Defense, World Premier International Research Center Immunology Frontier Research Center, Osaka, Japan; Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.

出版信息

J Allergy Clin Immunol. 2016 Jul;138(1):28-36. doi: 10.1016/j.jaci.2016.05.009. Epub 2016 May 24.

Abstract

Inflammasomes detect pathogen-associated molecular patterns to induce inflammatory innate immune responses and play a key role in host defense against infectious agents. However, inflammasomes are often wrongly activated by metabolites, amyloids, and environmental irritants. This induces massive inflammation, causing severe tissue damage, and results in the development of inflammatory diseases. Hence cellular machineries regulating both "activation" and "inactivation" of inflammasomes are definitely important. Recent studies have shown that autophagy, an intracellular degradation system associated with maintenance of cellular homeostasis, plays a key role in inflammasome inactivation. Notably, autophagy deficiency caused by gene mutation disrupts organelle elimination and thus induces aberrant activation of inflammasomes, leading to severe tissue damage. Here we review recent findings regarding the involvement of autophagy in the regulation of inflammasome activation and development of inflammatory disorders.

摘要

炎症小体检测病原体相关分子模式,诱导炎症性先天免疫反应,并在宿主防御感染因子中发挥关键作用。然而,炎症小体经常被代谢物、淀粉样物质和环境刺激物错误激活。这会引起大量炎症,导致严重的组织损伤,并导致炎症性疾病的发展。因此,调节炎症小体“激活”和“失活”的细胞机制肯定很重要。最近的研究表明,自噬是一种与维持细胞内稳态相关的细胞内降解系统,在炎症小体失活中发挥关键作用。值得注意的是,基因突变导致的自噬缺陷会破坏细胞器的清除,从而导致炎症小体异常激活,导致严重的组织损伤。在这里,我们综述了自噬在调节炎症小体激活和炎症性疾病发展中的作用的最新发现。

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