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本文引用的文献

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Role of metabolic reprogramming in pro-inflammatory cytokine secretion from LPS or silica-activated macrophages.代谢重编程在 LPS 或二氧化硅激活的巨噬细胞中促炎细胞因子分泌中的作用。
Front Immunol. 2022 Oct 21;13:936167. doi: 10.3389/fimmu.2022.936167. eCollection 2022.
2
Macrophage-mediated immune response aggravates hearing disfunction caused by the disorder of mitochondrial dynamics in cochlear hair cells.巨噬细胞介导的免疫反应会加重由耳蜗毛细胞线粒体动力学紊乱所导致的听力功能障碍。
Hum Mol Genet. 2023 Mar 20;32(7):1137-1151. doi: 10.1093/hmg/ddac270.
3
Redox regulation of the immune response.氧化还原调节免疫反应。
Cell Mol Immunol. 2022 Oct;19(10):1079-1101. doi: 10.1038/s41423-022-00902-0. Epub 2022 Sep 2.
4
The IRG1/itaconate/TFEB axis: A new weapon in macrophage antibacterial defense.IRG1/衣康酸/TFEB 轴:巨噬细胞抗菌防御的新武器。
Mol Cell. 2022 Aug 4;82(15):2732-2734. doi: 10.1016/j.molcel.2022.06.009.
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Gstm1/Gstt1 is essential for reducing cisplatin ototoxicity in CBA/CaJ mice.GSTM1/GSTT1 对于降低 CBA/CaJ 小鼠顺铂耳毒性至关重要。
FASEB J. 2022 Jun;36(6):e22373. doi: 10.1096/fj.202200324R.
6
Age-Related Hearing Loss Is Accompanied by Chronic Inflammation in the Cochlea and the Cochlear Nucleus.年龄相关性听力损失伴有耳蜗和耳蜗核的慢性炎症。
Front Aging Neurosci. 2022 Mar 28;14:846804. doi: 10.3389/fnagi.2022.846804. eCollection 2022.
7
Activation of Rictor/mTORC2 signaling acts as a pivotal strategy to protect against sensorineural hearing loss.激活Rictor/mTORC2信号传导是预防感音神经性听力损失的关键策略。
Proc Natl Acad Sci U S A. 2022 Mar 8;119(10):e2107357119. doi: 10.1073/pnas.2107357119. Epub 2022 Mar 1.
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Itaconate and itaconate derivatives target JAK1 to suppress alternative activation of macrophages.衣康酸盐和衣康酸盐衍生物靶向 JAK1 以抑制巨噬细胞的替代激活。
Cell Metab. 2022 Mar 1;34(3):487-501.e8. doi: 10.1016/j.cmet.2022.02.002.
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Blockage of citrate export prevents TCA cycle fragmentation via Irg1 inactivation.柠檬酸外排受阻通过 Irg1 失活防止 TCA 循环碎片化。
Cell Rep. 2022 Feb 15;38(7):110391. doi: 10.1016/j.celrep.2022.110391.
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Cytosolic escape of mitochondrial DNA triggers cGAS-STING-NLRP3 axis-dependent nucleus pulposus cell pyroptosis.线粒体DNA的胞质逃逸触发cGAS-STING-NLRP3轴依赖性的髓核细胞焦亡。
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线粒体对固有免疫中巨噬细胞的调节作用及巨噬细胞在耳蜗炎症中的多种作用。

Mitochondrial Regulation of Macrophages in Innate Immunity and Diverse Roles of Macrophages During Cochlear Inflammation.

机构信息

Department of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.

Shandong Provincial Hospital, Shandong First Medical University, Jinan, 250000, China.

出版信息

Neurosci Bull. 2024 Feb;40(2):255-267. doi: 10.1007/s12264-023-01085-y. Epub 2023 Jun 30.

DOI:10.1007/s12264-023-01085-y
PMID:37391607
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10838870/
Abstract

Macrophages are essential components of the innate immune system and constitute a non-specific first line of host defense against pathogens and inflammation. Mitochondria regulate macrophage activation and innate immune responses in various inflammatory diseases, including cochlear inflammation. The distribution, number, and morphological characteristics of cochlear macrophages change significantly across different inner ear regions under various pathological conditions, including noise exposure, ototoxicity, and age-related degeneration. However, the exact mechanism underlying the role of mitochondria in macrophages in auditory function remains unclear. Here, we summarize the major factors and mitochondrial signaling pathways (e.g., metabolism, mitochondrial reactive oxygen species, mitochondrial DNA, and the inflammasome) that influence macrophage activation in the innate immune response. In particular, we focus on the properties of cochlear macrophages, activated signaling pathways, and the secretion of inflammatory cytokines after acoustic injury. We hope this review will provide new perspectives and a basis for future research on cochlear inflammation.

摘要

巨噬细胞是先天免疫系统的重要组成部分,构成了宿主防御病原体和炎症的非特异性第一道防线。线粒体调节各种炎症性疾病中巨噬细胞的激活和先天免疫反应,包括耳蜗炎症。在不同的病理条件下,包括噪声暴露、耳毒性和与年龄相关的退化,不同内耳区域的耳蜗巨噬细胞的分布、数量和形态特征发生显著变化。然而,线粒体在巨噬细胞中在听觉功能中的作用的确切机制尚不清楚。在这里,我们总结了影响先天免疫反应中巨噬细胞激活的主要因素和线粒体信号通路(例如代谢、线粒体活性氧、线粒体 DNA 和炎性体)。特别是,我们重点介绍耳蜗巨噬细胞的特性、激活的信号通路以及声损伤后炎症细胞因子的分泌。我们希望本综述将为耳蜗炎症的未来研究提供新的视角和基础。