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巨噬细胞驱动的心脏炎症与修复:从稳态和心肌梗死中获得的认识。

Macrophage-driven cardiac inflammation and healing: insights from homeostasis and myocardial infarction.

机构信息

Department of Cardiology, Zhongda Hospital, School of Medicine, Southeast University, No. 87, Dingjiaqiao, Nanjing, 210009, China.

Department of Cardiology, Yancheng No. 1 People's Hospital, No. 66 South Renmin Road, Yancheng, 224000, China.

出版信息

Cell Mol Biol Lett. 2023 Oct 19;28(1):81. doi: 10.1186/s11658-023-00491-4.

DOI:10.1186/s11658-023-00491-4
PMID:37858035
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10585879/
Abstract

Early and prompt reperfusion therapy has markedly improved the survival rates among patients enduring myocardial infarction (MI). Nonetheless, the resulting adverse remodeling and the subsequent onset of heart failure remain formidable clinical management challenges and represent a primary cause of disability in MI patients worldwide. Macrophages play a crucial role in immune system regulation and wield a profound influence over the inflammatory repair process following MI, thereby dictating the degree of myocardial injury and the subsequent pathological remodeling. Despite numerous previous biological studies that established the classical polarization model for macrophages, classifying them as either M1 pro-inflammatory or M2 pro-reparative macrophages, this simplistic categorization falls short of meeting the precision medicine standards, hindering the translational advancement of clinical research. Recently, advances in single-cell sequencing technology have facilitated a more profound exploration of macrophage heterogeneity and plasticity, opening avenues for the development of targeted interventions to address macrophage-related factors in the aftermath of MI. In this review, we provide a summary of macrophage origins, tissue distribution, classification, and surface markers. Furthermore, we delve into the multifaceted roles of macrophages in maintaining cardiac homeostasis and regulating inflammation during the post-MI period.

摘要

早期和及时的再灌注治疗显著提高了心肌梗死(MI)患者的生存率。然而,由此产生的不良重构以及随后发生的心力衰竭仍然是极具挑战性的临床管理难题,也是全球 MI 患者残疾的主要原因。巨噬细胞在免疫系统调节中发挥着关键作用,对 MI 后的炎症修复过程有着深远的影响,从而决定了心肌损伤的程度和随后的病理性重构。尽管之前有许多生物学研究建立了巨噬细胞的经典极化模型,将其分为 M1 促炎或 M2 修复型巨噬细胞,但这种简单的分类方法不符合精准医学的标准,阻碍了临床研究的转化进展。最近,单细胞测序技术的进步促进了对巨噬细胞异质性和可塑性的更深入探索,为开发针对 MI 后巨噬细胞相关因素的靶向干预措施开辟了道路。在这篇综述中,我们总结了巨噬细胞的起源、组织分布、分类和表面标志物。此外,我们还深入探讨了巨噬细胞在维持心脏内稳态和调节 MI 后炎症过程中的多方面作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed2/10585879/55932b2994a3/11658_2023_491_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed2/10585879/84eafc23a041/11658_2023_491_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed2/10585879/32896f397a21/11658_2023_491_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed2/10585879/e20319763407/11658_2023_491_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed2/10585879/55932b2994a3/11658_2023_491_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed2/10585879/84eafc23a041/11658_2023_491_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed2/10585879/32896f397a21/11658_2023_491_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed2/10585879/e20319763407/11658_2023_491_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ed2/10585879/55932b2994a3/11658_2023_491_Fig4_HTML.jpg

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