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应激颗粒:感染性和炎症性疾病的潜在治疗靶点。

Stress granules: potential therapeutic targets for infectious and inflammatory diseases.

机构信息

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.

Department of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.

出版信息

Front Immunol. 2023 May 2;14:1145346. doi: 10.3389/fimmu.2023.1145346. eCollection 2023.

DOI:10.3389/fimmu.2023.1145346
PMID:37205103
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10185834/
Abstract

Eukaryotic cells are stimulated by external pressure such as that derived from heat shock, oxidative stress, nutrient deficiencies, or infections, which induce the formation of stress granules (SGs) that facilitates cellular adaptation to environmental pressures. As aggregated products of the translation initiation complex in the cytoplasm, SGs play important roles in cell gene expression and homeostasis. Infection induces SGs formation. Specifically, a pathogen that invades a host cell leverages the host cell translation machinery to complete the pathogen life cycle. In response, the host cell suspends translation, which leads to SGs formation, to resist pathogen invasion. This article reviews the production and function of SGs, the interaction between SGs and pathogens, and the relationship between SGs and pathogen-induced innate immunity to provide directions for further research into anti-infection and anti-inflammatory disease strategies.

摘要

真核细胞受到外部压力的刺激,如热休克、氧化应激、营养缺乏或感染等,这些压力会诱导应激颗粒(SGs)的形成,从而促进细胞适应环境压力。作为细胞质中翻译起始复合物的聚集产物,SGs 在细胞基因表达和稳态中发挥着重要作用。感染诱导 SGs 的形成。具体来说,入侵宿主细胞的病原体利用宿主细胞的翻译机制来完成病原体的生命周期。作为回应,宿主细胞暂停翻译,导致 SGs 的形成,以抵抗病原体的入侵。本文综述了 SGs 的产生和功能、SGs 与病原体的相互作用以及 SGs 与病原体诱导的固有免疫之间的关系,为进一步研究抗感染和抗炎性疾病的策略提供了方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d72a/10185834/b90e5aa61f5a/fimmu-14-1145346-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d72a/10185834/74f863c6d4d4/fimmu-14-1145346-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d72a/10185834/7dd60ae81fc9/fimmu-14-1145346-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d72a/10185834/b90e5aa61f5a/fimmu-14-1145346-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d72a/10185834/74f863c6d4d4/fimmu-14-1145346-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d72a/10185834/7dd60ae81fc9/fimmu-14-1145346-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d72a/10185834/b90e5aa61f5a/fimmu-14-1145346-g003.jpg

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World J Gastroenterol. 2023 Feb 28;29(8):1315-1329. doi: 10.3748/wjg.v29.i8.1315.
2
Glucocorticoids enhance chemotherapy-driven stress granule assembly and impair granule dynamics, leading to cell death.糖皮质激素增强化疗诱导的应激颗粒组装并损害颗粒动力学,导致细胞死亡。
J Cell Sci. 2022 Jul 15;135(14). doi: 10.1242/jcs.259629. Epub 2022 Jul 26.
3
GADD34-mediated dephosphorylation of eIF2α facilitates pseudorabies virus replication by maintaining de novo protein synthesis.
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应激颗粒与细胞死亡:传染病中的相互作用及潜在治疗策略
Cell Death Dis. 2025 Jul 5;16(1):495. doi: 10.1038/s41419-025-07800-z.
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Connecting the Dots: Stress Granule and Cardiovascular Diseases.追根溯源:应激颗粒与心血管疾病
J Cardiovasc Transl Res. 2025 Apr 14. doi: 10.1007/s12265-025-10619-w.
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