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炎症消退:对动脉粥样硬化的影响。

Inflammation Resolution: Implications for Atherosclerosis.

机构信息

Department of Medicine, Division of Cardiovascular Medicine, Vanderbilt Institute for Infection, Immunology and Inflammation, Department of Molecular Physiology and Biophysics and Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN.

出版信息

Circ Res. 2022 Jan 7;130(1):130-148. doi: 10.1161/CIRCRESAHA.121.319822.

DOI:10.1161/CIRCRESAHA.121.319822
PMID:34995137
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8842990/
Abstract

Resolution is an active and highly coordinated process that occurs in response to inflammation to limit tissue damage and promote repair. When the resolution program fails, inflammation persists. It is now understood that failed resolution is a major underlying cause of many chronic inflammatory diseases. Here, we will review the major failures of resolution in atherosclerosis, including the imbalance of proinflammatory to pro-resolving mediator production, impaired clearance of dead cells, and functional changes in immune cells that favor ongoing inflammation. In addition, we will briefly discuss new concepts that are emerging as possible regulators of resolution and highlight the translational significance for the field.

摘要

分辨率是一个主动和高度协调的过程,发生在响应炎症,以限制组织损伤和促进修复。当分辨率程序失败时,炎症持续存在。现在人们已经了解到,分辨率的失败是许多慢性炎症性疾病的主要潜在原因。在这里,我们将回顾动脉粥样硬化中分辨率的主要失败,包括促炎介质到促分辨率介质产生的失衡,死亡细胞清除受损,以及有利于持续炎症的免疫细胞的功能变化。此外,我们还将简要讨论作为分辨率可能调节剂的新概念,并强调该领域的转化意义。

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2
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Platelet Membrane Biomimetic Chemiluminescent Nanoparticles for Targeted Therapy of Atherosclerosis.用于动脉粥样硬化靶向治疗的血小板膜仿生化学发光纳米颗粒
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Harnessing extracellular vesicles to tame inflammation: a new strategy for atherosclerosis therapy.利用细胞外囊泡控制炎症:动脉粥样硬化治疗的新策略。

本文引用的文献

1
Efferocytosis induces macrophage proliferation to help resolve tissue injury.吞噬作用可诱导巨噬细胞增殖,以帮助组织损伤修复。
Cell Metab. 2021 Dec 7;33(12):2445-2463.e8. doi: 10.1016/j.cmet.2021.10.015. Epub 2021 Nov 15.
2
The resolvin D1 receptor GPR32 transduces inflammation resolution and atheroprotection.解析素 D1 受体 GPR32 转导炎症缓解和动脉保护。
J Clin Invest. 2021 Dec 15;131(24). doi: 10.1172/JCI142883.
3
Non-canonical glutamine transamination sustains efferocytosis by coupling redox buffering to oxidative phosphorylation.
Front Immunol. 2025 Jun 18;16:1625958. doi: 10.3389/fimmu.2025.1625958. eCollection 2025.
4
A bibliometric analysis of macrophage-associated immune regulation in atherosclerosis: advances in the mechanisms of pathogenesis.动脉粥样硬化中巨噬细胞相关免疫调节的文献计量分析:发病机制研究进展
Front Immunol. 2025 Jun 12;16:1559360. doi: 10.3389/fimmu.2025.1559360. eCollection 2025.
5
Inhibition of USP5 Attenuates Atherosclerosis by Suppressing PDCD4-Mediated Endothelial Dysfunction: Evidence from In Vitro HUVEC and In Vivo Models.抑制USP5通过抑制PDCD4介导的内皮功能障碍减轻动脉粥样硬化:来自体外人脐静脉内皮细胞和体内模型的证据
Cardiovasc Toxicol. 2025 Jun 26. doi: 10.1007/s12012-025-10007-5.
6
Human CD36: Gene Regulation, Protein Function, and Its Role in Atherosclerosis Pathogenesis.人类CD36:基因调控、蛋白质功能及其在动脉粥样硬化发病机制中的作用。
Genes (Basel). 2025 Jun 13;16(6):705. doi: 10.3390/genes16060705.
7
Calcium Signaling Dynamics in Vascular Cells and Their Dysregulation in Vascular Disease.血管细胞中的钙信号动力学及其在血管疾病中的失调
Biomolecules. 2025 Jun 18;15(6):892. doi: 10.3390/biom15060892.
8
Circular RNA-Sirt1 sponges miR-27b-3p to protect vascular smooth muscle cell injury during atherosclerosis through regulating the glutamine metabolism pathway.环状RNA-Sirt1通过调节谷氨酰胺代谢途径,海绵化miR-27b-3p以保护动脉粥样硬化过程中的血管平滑肌细胞损伤。
Cytotechnology. 2025 Aug;77(4):122. doi: 10.1007/s10616-025-00759-x. Epub 2025 Jun 11.
9
Inflammation and depression: an evolutionary framework for the role of physical activity and exercise.炎症与抑郁:身体活动和运动作用的进化框架
Front Psychol. 2025 May 29;16:1554062. doi: 10.3389/fpsyg.2025.1554062. eCollection 2025.
10
Insights Into Heart-Tumor Interactions in Heart Failure.心力衰竭中心脏与肿瘤相互作用的见解
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非经典谷氨酰胺转氨酶通过将氧化还原缓冲与氧化磷酸化偶联来维持吞噬作用。
Nat Metab. 2021 Oct;3(10):1313-1326. doi: 10.1038/s42255-021-00471-y. Epub 2021 Oct 14.
4
Long Noncoding RNA Controls Advanced Atherosclerotic Lesion Formation and Plaque Destabilization.长链非编码 RNA 控制动脉粥样硬化病变的形成和斑块不稳定。
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5
Atherosclerosis is a major human killer and non-resolving inflammation is a prime suspect.动脉粥样硬化是人类的主要杀手,而未解决的炎症是主要嫌疑犯。
Cardiovasc Res. 2021 Nov 22;117(13):2563-2574. doi: 10.1093/cvr/cvab309.
6
How the immune system shapes atherosclerosis: roles of innate and adaptive immunity.免疫系统如何塑造动脉粥样硬化:先天免疫和适应性免疫的作用。
Nat Rev Immunol. 2022 Apr;22(4):251-265. doi: 10.1038/s41577-021-00584-1. Epub 2021 Aug 13.
7
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Cell Death Dis. 2021 Aug 10;12(8):782. doi: 10.1038/s41419-021-04054-3.
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Circ Res. 2021 Aug 20;129(5):530-546. doi: 10.1161/CIRCRESAHA.121.319313. Epub 2021 Jul 22.
9
Myeloid-associated lipin-1 transcriptional co-regulatory activity is atheroprotective.髓系相关脂肪酶 lipin-1 的转录共调节活性具有抗动脉粥样硬化作用。
Atherosclerosis. 2021 Aug;330:76-84. doi: 10.1016/j.atherosclerosis.2021.06.927. Epub 2021 Jul 1.
10
Pyroptosis in the Initiation and Progression of Atherosclerosis.细胞焦亡在动脉粥样硬化的起始与进展过程中的作用
Front Pharmacol. 2021 May 26;12:652963. doi: 10.3389/fphar.2021.652963. eCollection 2021.