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

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...

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Autores principales: Zuo, Wenjie, Sun, Renhua, Ji, Zhenjun, Ma, Genshan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10585879/
https://www.ncbi.nlm.nih.gov/pubmed/37858035
http://dx.doi.org/10.1186/s11658-023-00491-4
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author Zuo, Wenjie
Sun, Renhua
Ji, Zhenjun
Ma, Genshan
author_facet Zuo, Wenjie
Sun, Renhua
Ji, Zhenjun
Ma, Genshan
author_sort Zuo, Wenjie
collection PubMed
description 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.
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spelling pubmed-105858792023-10-20 Macrophage-driven cardiac inflammation and healing: insights from homeostasis and myocardial infarction Zuo, Wenjie Sun, Renhua Ji, Zhenjun Ma, Genshan Cell Mol Biol Lett Review 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. BioMed Central 2023-10-19 /pmc/articles/PMC10585879/ /pubmed/37858035 http://dx.doi.org/10.1186/s11658-023-00491-4 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Review
Zuo, Wenjie
Sun, Renhua
Ji, Zhenjun
Ma, Genshan
Macrophage-driven cardiac inflammation and healing: insights from homeostasis and myocardial infarction
title Macrophage-driven cardiac inflammation and healing: insights from homeostasis and myocardial infarction
title_full Macrophage-driven cardiac inflammation and healing: insights from homeostasis and myocardial infarction
title_fullStr Macrophage-driven cardiac inflammation and healing: insights from homeostasis and myocardial infarction
title_full_unstemmed Macrophage-driven cardiac inflammation and healing: insights from homeostasis and myocardial infarction
title_short Macrophage-driven cardiac inflammation and healing: insights from homeostasis and myocardial infarction
title_sort macrophage-driven cardiac inflammation and healing: insights from homeostasis and myocardial infarction
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10585879/
https://www.ncbi.nlm.nih.gov/pubmed/37858035
http://dx.doi.org/10.1186/s11658-023-00491-4
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