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自噬与炎症

Autophagy and inflammation.

作者信息

Qian Mengjia, Fang Xiaocong, Wang Xiangdong

机构信息

Zhongshan Hospital Institute of Clinical Science, Shanghai Institute of Clinical Bioinformatics, Fudan University Medical School, Shanghai, China.

出版信息

Clin Transl Med. 2017 Dec;6(1):24. doi: 10.1186/s40169-017-0154-5. Epub 2017 Jul 26.

DOI:10.1186/s40169-017-0154-5
PMID:28748360
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5529308/
Abstract

Autophagy is a homeostatic mechanism involved in the disposal of damaged organelles, denatured proteins as well as invaded pathogens through a lysosomal degradation pathway. Recently, increasing evidences have demonstrated its role in both innate and adaptive immunity, and thereby influence the pathogenesis of inflammatory diseases. The detection of autophagy machinery facilitated the measurement of autophagy during physiological and pathophysiological processes. Autophagy plays critical roles in inflammation through influencing the development, homeostasis and survival of inflammatory cells, including macrophages, neutrophils and lymphocytes; effecting the transcription, processing and secretion of a number of cytokines, as well as being regulated by cytokines. Recently, autophagy-dependent mechanisms have been studied in the pathogenesis of several inflammatory diseases, including infectious diseases, Crohn's disease, cystic fibrosis, pulmonary hypertension, chronic obstructive pulmonary diseases and so on. These studies suggested that modulation of autophagy might lead to therapeutic interventions for diseases associated with inflammation. Here we highlight recent advances in investigating the roles of autophagy in inflammation as well as inflammatory diseases.

摘要

自噬是一种稳态机制,通过溶酶体降解途径参与受损细胞器、变性蛋白质以及入侵病原体的清除。最近,越来越多的证据表明其在固有免疫和适应性免疫中均发挥作用,进而影响炎症性疾病的发病机制。自噬机制的检测有助于在生理和病理生理过程中对自噬进行测量。自噬通过影响包括巨噬细胞、中性粒细胞和淋巴细胞在内的炎症细胞的发育、稳态和存活;影响多种细胞因子的转录、加工和分泌,以及受细胞因子调节,在炎症中发挥关键作用。最近,自噬依赖性机制已在包括传染病、克罗恩病、囊性纤维化、肺动脉高压、慢性阻塞性肺疾病等多种炎症性疾病的发病机制中得到研究。这些研究表明,调节自噬可能为与炎症相关的疾病带来治疗干预措施。在此,我们重点介绍自噬在炎症以及炎症性疾病中作用的最新研究进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d963/5529308/c9b3d062a7e4/40169_2017_154_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d963/5529308/7ab4a0210f81/40169_2017_154_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d963/5529308/5b78ea9f7ee5/40169_2017_154_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d963/5529308/c9b3d062a7e4/40169_2017_154_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d963/5529308/7ab4a0210f81/40169_2017_154_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d963/5529308/5b78ea9f7ee5/40169_2017_154_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d963/5529308/c9b3d062a7e4/40169_2017_154_Fig3_HTML.jpg

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Onco Targets Ther. 2017 Jun 6;10:2865-2871. doi: 10.2147/OTT.S95267. eCollection 2017.
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Autophagy downstream of endosomal Toll-like receptor signaling in macrophages is a key mechanism for resistance to infection.巨噬细胞内体Toll样受体信号下游的自噬是抵抗感染的关键机制。
J Biol Chem. 2017 Aug 11;292(32):13087-13096. doi: 10.1074/jbc.M117.780981. Epub 2017 Jun 12.
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founder mutation causes protein trafficking defects in Chinese patients with cystic fibrosis.
Mechanistic and therapeutic insights into the function of different cell death modalities in rheumatoid arthritis: emphasis on the crosstalk with non-coding RNAs.
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Front Immunol. 2025 Jul 23;16:1620209. doi: 10.3389/fimmu.2025.1620209. eCollection 2025.
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MAB_0676c-induced enhanced IL-10 production inhibits the autophagic flux via the MTOR/RUBCN pathway.MAB_0676c诱导的IL-10产生增强通过MTOR/RUBCN途径抑制自噬通量。
Virulence. 2025 Dec;16(1):2529493. doi: 10.1080/21505594.2025.2529493. Epub 2025 Jul 10.
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Native Lactobacillus and Bifidobacterium probiotics modulate autophagy genes and exert anti-inflammatory effect.天然的乳酸杆菌和双歧杆菌益生菌可调节自噬基因并发挥抗炎作用。
Sci Rep. 2025 Jul 11;15(1):25006. doi: 10.1038/s41598-025-09596-6.
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ALS-associated TDP-43 aggregates drive innate and adaptive immune cell activation.与肌萎缩侧索硬化症相关的TDP-43聚集体驱动先天性和适应性免疫细胞激活。
iScience. 2025 May 13;28(6):112648. doi: 10.1016/j.isci.2025.112648. eCollection 2025 Jun 20.
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Genome-wide association study and transcriptomic analysis reveal the crucial role of in resistance to visceral white-nodules disease in .全基因组关联研究和转录组分析揭示了[具体内容]在[具体对象]对内脏白色结节病抗性中的关键作用。
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TLR7 Mediates HIV-1 Tat-Induced Cellular Senescence in Human Astrocytes.Toll样受体7介导HIV-1反式激活因子诱导的人星形胶质细胞衰老
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Antioxidants (Basel). 2025 Apr 1;14(4):428. doi: 10.3390/antiox14040428.
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