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胞葬作用在缺血性卒中中的作用及视网膜病变的启示

The role of efferocytosis in ischemic stroke and insights from retinopathy.

作者信息

Morris Carol A, Sadek Mohamed A, Modi Pooja, Abdelnaem Seif, Rusch Nancy J, Shosha Esraa, Fouda Abdelrahman Y

机构信息

Department of Pharmacology & Toxicology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR, USA.

Department of Pharmacology & Toxicology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR, USA; Department of Clinical Pharmacy, Faculty of Pharmacy, Cairo University, Cairo, Egypt; Department of Pharmacology & Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt.

出版信息

Trends Neurosci. 2025 Jul 15. doi: 10.1016/j.tins.2025.06.002.

DOI:10.1016/j.tins.2025.06.002
PMID:40670232
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12276843/
Abstract

Efferocytosis, the phagocytic removal of dead cells by microglia and macrophages, was recently recognized as a critical process in the resolution of inflammation and tissue repair following ischemic stroke. In this review, we examine the pathways involved in efferocytosis after stroke, including the recognition and engulfment of apoptotic cells and the modulation of inflammatory responses. We elaborate on the pathways regulating efferocytosis and discuss how dysregulated efferocytosis can contribute to secondary injury and neurological deficits. Furthermore, we explore valuable mechanisms gleaned from retinopathy, a condition with parallels to ischemic stroke in terms of cellular death and immune responses. We then discuss phagocytosis assays used in brain and retina research. Finally, we highlight future perspectives on, and outstanding questions related to, efferocytosis in stroke.

摘要

胞葬作用,即小胶质细胞和巨噬细胞对死细胞的吞噬清除作用,最近被认为是缺血性中风后炎症消退和组织修复过程中的一个关键过程。在这篇综述中,我们研究了中风后胞葬作用所涉及的途径,包括凋亡细胞的识别和吞噬以及炎症反应的调节。我们详细阐述了调节胞葬作用的途径,并讨论了失调的胞葬作用如何导致继发性损伤和神经功能缺损。此外,我们探索了从视网膜病变中获得的有价值的机制,视网膜病变在细胞死亡和免疫反应方面与缺血性中风有相似之处。然后我们讨论了在脑和视网膜研究中使用的吞噬试验。最后,我们强调了中风中胞葬作用的未来前景以及相关的突出问题。

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本文引用的文献

1
Repair-associated macrophages increase after early-phase microglia attenuation to promote ischemic stroke recovery.早期小胶质细胞衰减后,与修复相关的巨噬细胞增加,以促进缺血性中风的恢复。
Nat Commun. 2025 Mar 31;16(1):3089. doi: 10.1038/s41467-025-58254-y.
2
Detrimental influence of Arginase-1 in infiltrating macrophages on poststroke functional recovery and inflammatory milieu.精氨酸酶-1在浸润巨噬细胞中对中风后功能恢复和炎症微环境的有害影响。
Proc Natl Acad Sci U S A. 2025 Feb 18;122(7):e2413484122. doi: 10.1073/pnas.2413484122. Epub 2025 Feb 14.
3
Ischemic Conditioning Promotes Transneuronal Survival and Stroke Recovery via CD36-Mediated Efferocytosis.缺血预处理通过CD36介导的胞葬作用促进跨神经元存活和中风恢复。
Circ Res. 2025 Feb 28;136(5):e34-e51. doi: 10.1161/CIRCRESAHA.124.325428. Epub 2025 Jan 31.
4
Enhancing Neuron Activity Promotes Functional Recovery by Inhibiting Microglia-Mediated Synapse Elimination After Stroke.增强神经元活性通过抑制中风后小胶质细胞介导的突触消除促进功能恢复。
Stroke. 2025 Feb;56(2):505-516. doi: 10.1161/STROKEAHA.124.049265. Epub 2025 Jan 8.
5
Orchestrating the frontline: HDAC3-miKO recruits macrophage reinforcements for accelerated myelin debris clearance after stroke.协调前线:HDAC3-miKO招募巨噬细胞援军以加速中风后髓鞘碎片清除
Theranostics. 2025 Jan 1;15(2):632-655. doi: 10.7150/thno.103449. eCollection 2025.
6
Efferocytosis: the resolution of inflammation in cardiovascular and cerebrovascular disease.胞葬作用:心血管和脑血管疾病中炎症的消退
Front Immunol. 2024 Nov 26;15:1485222. doi: 10.3389/fimmu.2024.1485222. eCollection 2024.
7
Sigma-1 receptor signaling: A potential therapeutic approach for ischemic stroke.西格玛-1受体信号传导:缺血性中风的一种潜在治疗方法。
J Cereb Blood Flow Metab. 2024 Dec;44(12):1430-1440. doi: 10.1177/0271678X241281547. Epub 2024 Sep 9.
8
Electroacupuncture reduces inflammatory damage following cerebral ischemia-reperfusion by enhancing ABCA1-mediated efferocytosis in M2 microglia.电针对脑缺血再灌注后炎症损伤的作用机制:通过增强 M2 型小胶质细胞 ABCA1 介导的噬作用。
Mol Brain. 2024 Sep 2;17(1):61. doi: 10.1186/s13041-024-01135-0.
9
Microglia through MFG-E8 signaling decrease the density of degenerating neurons and protect the brain from the development of cortical infarction after stroke.小胶质细胞通过 MFG-E8 信号减少变性神经元的密度,并保护大脑免受中风后皮质梗死的发展。
PLoS One. 2024 Aug 7;19(8):e0308464. doi: 10.1371/journal.pone.0308464. eCollection 2024.
10
S100A9 deletion in microglia/macrophages ameliorates brain injury through the STAT6/PPARγ pathway in ischemic stroke.小胶质细胞/巨噬细胞 S100A9 缺失通过 STAT6/PPARγ 通路减轻缺血性脑卒中的脑损伤。
CNS Neurosci Ther. 2024 Aug;30(8):e14881. doi: 10.1111/cns.14881.