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中性粒细胞在心肌梗死后修复过程中的信号转导。

Neutrophil signaling during myocardial infarction wound repair.

机构信息

Department of Cellular and Integrative Physiology, Center for Heart and Vascular Research, University of Nebraska Medical Center, Omaha, NE 68198, USA; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS 39216, USA; Research Service, Nebraska-Western Iowa Health Care System, Omaha, NE 68198, USA.

Department of Cellular and Integrative Physiology, Center for Heart and Vascular Research, University of Nebraska Medical Center, Omaha, NE 68198, USA; Research Service, Nebraska-Western Iowa Health Care System, Omaha, NE 68198, USA.

出版信息

Cell Signal. 2021 Jan;77:109816. doi: 10.1016/j.cellsig.2020.109816. Epub 2020 Oct 24.

DOI:10.1016/j.cellsig.2020.109816
PMID:33122000
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7718402/
Abstract

Neutrophils are key effector cells of the innate immune system, serving as a first line of defense in the response to injury and playing essential roles in the wound healing process. Following myocardial infarction (MI), neutrophils infiltrate into the infarct region to propagate inflammation and begin the initial phase of cardiac wound repair. Pro-inflammatory neutrophils release proteases to degrade extracellular matrix (ECM), a necessary step for the removal of necrotic myocytes as a prelude for scar formation. Neutrophils transition their phenotype over time to regulate MI inflammation resolution and stabilize scar formation. Neutrophils contribute to the evolution from inflammation to resolution and scar formation by serving anti-inflammatory and repair functions. As anti-inflammatory cells, neutrophils contribute ECM proteins during scar formation, in particular fibronectin, galectin-3, and vimentin. The diverse and polarizing functions that contribute to MI wound repair make this innate immune cell a viable target to improve MI outcomes. Thus, understanding the signaling involved in neutrophil physiology in the context of MI may help to identify novel therapeutic targets.

摘要

中性粒细胞是先天免疫系统的关键效应细胞,作为对损伤的反应的第一道防线,在伤口愈合过程中发挥着重要作用。心肌梗死后(MI),中性粒细胞浸润到梗死区域,引发炎症,并开始心脏伤口修复的初始阶段。促炎中性粒细胞释放蛋白酶来降解细胞外基质(ECM),这是去除坏死心肌细胞的必要步骤,也是形成瘢痕的前奏。中性粒细胞随着时间的推移改变其表型,以调节 MI 炎症的消退和瘢痕的形成。中性粒细胞通过发挥抗炎和修复功能,有助于从炎症向消退和瘢痕形成的演变。作为抗炎细胞,中性粒细胞在瘢痕形成过程中贡献细胞外基质蛋白,特别是纤维连接蛋白、半乳糖凝集素-3 和波形蛋白。这些有助于 MI 伤口修复的多样化和极化功能使这种先天免疫细胞成为改善 MI 结局的可行靶点。因此,了解 MI 背景下中性粒细胞生理学中的信号转导可能有助于确定新的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a46/7718402/9ef2d675f988/nihms-1644189-f0006.jpg
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