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自噬与炎症:在病毒感染中的调控作用。

Autophagy and Inflammation: Regulatory Roles in Viral Infections.

机构信息

School of Medicine, Jiamusi University, Jiamusi 154007, China.

School of Medicine, Dalian University, Dalian 116622, China.

出版信息

Biomolecules. 2023 Sep 27;13(10):1454. doi: 10.3390/biom13101454.

DOI:10.3390/biom13101454
PMID:37892135
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10604974/
Abstract

Autophagy is a highly conserved intracellular degradation pathway in eukaryotic organisms, playing an adaptive role in various pathophysiological processes throughout evolution. Inflammation is the immune system's response to external stimuli and tissue damage. However, persistent inflammatory reactions can lead to a range of inflammatory diseases and cancers. The interaction between autophagy and inflammation is particularly evident during viral infections. As a crucial regulator of inflammation, autophagy can either promote or inhibit the occurrence of inflammatory responses. In turn, inflammation can establish negative feedback loops by modulating autophagy to suppress excessive inflammatory reactions. This interaction is pivotal in the pathogenesis of viral diseases. Therefore, elucidating the regulatory roles of autophagy and inflammation in viral infections will significantly enhance our understanding of the mechanisms underlying related diseases. Furthermore, it will provide new insights and theoretical foundations for disease prevention, treatment, and drug development.

摘要

自噬是真核生物中一种高度保守的细胞内降解途径,在进化过程中的各种病理生理过程中发挥适应性作用。炎症是免疫系统对外部刺激和组织损伤的反应。然而,持续的炎症反应会导致一系列炎症性疾病和癌症。自噬和炎症之间的相互作用在病毒感染中尤为明显。自噬作为炎症的关键调节因子,可以促进或抑制炎症反应的发生。反过来,炎症可以通过调节自噬来抑制过度的炎症反应,建立负反馈回路。这种相互作用在病毒疾病的发病机制中至关重要。因此,阐明自噬和炎症在病毒感染中的调节作用将极大地增强我们对相关疾病发病机制的理解。此外,它将为疾病预防、治疗和药物开发提供新的见解和理论基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dc0/10604974/488d8115ba57/biomolecules-13-01454-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dc0/10604974/7ed6f9b8c13a/biomolecules-13-01454-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dc0/10604974/63528f168422/biomolecules-13-01454-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dc0/10604974/21ea91a0e987/biomolecules-13-01454-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dc0/10604974/4991389105b6/biomolecules-13-01454-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dc0/10604974/488d8115ba57/biomolecules-13-01454-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dc0/10604974/7ed6f9b8c13a/biomolecules-13-01454-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dc0/10604974/63528f168422/biomolecules-13-01454-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dc0/10604974/21ea91a0e987/biomolecules-13-01454-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dc0/10604974/4991389105b6/biomolecules-13-01454-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0dc0/10604974/488d8115ba57/biomolecules-13-01454-g005.jpg

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本文引用的文献

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Signal Transduct Target Ther. 2023 Mar 9;8(1):108. doi: 10.1038/s41392-023-01368-w.
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The role of autophagy in viral infections.自噬在病毒感染中的作用。
靶向 PNPO 抑制自噬流以抑制卵巢癌细胞生长并逆转紫杉醇耐药性。
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Echovirus 11 infection induces pyroptotic cell death by facilitating NLRP3 inflammasome activation.肠道病毒 11 感染通过促进 NLRP3 炎性小体激活诱导细胞发生细胞焦亡。
PLoS Pathog. 2022 Aug 26;18(8):e1010787. doi: 10.1371/journal.ppat.1010787. eCollection 2022 Aug.
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Targeting NLRP3-Mediated Neuroinflammation in Alzheimer's Disease Treatment.靶向 NLRP3 介导的神经炎症治疗阿尔茨海默病。
Int J Mol Sci. 2022 Aug 11;23(16):8979. doi: 10.3390/ijms23168979.
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USP22 suppresses the NLRP3 inflammasome by degrading NLRP3 via ATG5-dependent autophagy.USP22 通过依赖 ATG5 的自噬作用降解 NLRP3 来抑制 NLRP3 炎症小体。
Autophagy. 2023 Mar;19(3):873-885. doi: 10.1080/15548627.2022.2107314. Epub 2022 Aug 8.
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Autophagy at the intersection of aging, senescence, and cancer.自噬在衰老、衰老和癌症中的交汇。
Mol Oncol. 2022 Sep;16(18):3259-3275. doi: 10.1002/1878-0261.13269. Epub 2022 Jul 9.
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CCDC50 suppresses NLRP3 inflammasome activity by mediating autophagic degradation of NLRP3.CCDC50 通过介导 NLRP3 的自噬降解来抑制 NLRP3 炎症小体的活性。
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