[Role of macrophages in the pathogenesis of septic cardiomyopathy].

Q3 Medicine
Linke Zhang, Zhiling Zhao, Tingcui Li, Wen Li, Yuxin Leng, Qinggang Ge
{"title":"[Role of macrophages in the pathogenesis of septic cardiomyopathy].","authors":"Linke Zhang, Zhiling Zhao, Tingcui Li, Wen Li, Yuxin Leng, Qinggang Ge","doi":"10.3760/cma.j.cn121430-20240925-00797","DOIUrl":null,"url":null,"abstract":"<p><p>Sepsis is a life-threatening organ dysfunction caused by the body's dysregulated response to infection. Reversible myocardial dysfunction caused by sepsis is known as septic cardiomyopathy. A thorough understanding of the pathogenesis of septic cardiomyopathy is crucial for early intervention to prevent its progression and improve the success rate of sepsis treatment. At present, the research on the pathogenesis of septic cardiomyopathy mainly focuses on two aspects: the systemic neuroimmune mechanism and the local changes of cardiomyocytes. The former mainly includes the autonomic nervous dysfunction mainly caused by sympathetic overactivation and the inflammatory storm induced by immune response disorder. The latter covers the dysregulation of calcium homeostasis, mitochondrial dysfunction and energy metabolism disorder of cardiomyocytes. Immune dysfunction is one of the key factors that cause the poor prognosis of patients with septic cardiomyopathy. Macrophages are sentinel cells of the body's innate immunity. Cardiac macrophages have been confirmed to be one of the most heterogeneous immune cells in the heart. According to their origin and differentiation, they can be divided into bone marrow-derived tissue infiltrating macrophages and cardiac resident macrophages, which have roles of polarization, phagocytosis, regulation of inflammatory response, and participate in innate and adaptive immunity. In the occurrence and development of septic cardiomyopathy, cardiac macrophages recruited from the blood participate in balancing the inflammation and repair of myocardial tissue through the conversion of pro-inflammatory phenotype and anti-inflammatory phenotype. Cardiac resident macrophages mediate immune phagocytosis to maintain the local homeostasis of cardiomyocytes, and the glycometabolic reprogramming of macrophages regulates the release of inflammatory factors, while macrophage metabolic reprogramming regulates the release of inflammatory factors. A deeper understanding of the biological behavior of macrophages, and regulating the polarization, metabolism and phagocytosis of cardiac macrophages, could serve as new target for the prevention and treatment of septic cardiomyopathy. Therefore, this article reviews the key pathogenesis of septic cardiomyopathy and the role of macrophages of different origins and differentiation, revealing the possibility of developing new strategies for the prevention and treatment of septic cardiomyopathy.</p>","PeriodicalId":24079,"journal":{"name":"Zhonghua wei zhong bing ji jiu yi xue","volume":"37 3","pages":"305-309"},"PeriodicalIF":0.0000,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Zhonghua wei zhong bing ji jiu yi xue","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3760/cma.j.cn121430-20240925-00797","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0

Abstract

Sepsis is a life-threatening organ dysfunction caused by the body's dysregulated response to infection. Reversible myocardial dysfunction caused by sepsis is known as septic cardiomyopathy. A thorough understanding of the pathogenesis of septic cardiomyopathy is crucial for early intervention to prevent its progression and improve the success rate of sepsis treatment. At present, the research on the pathogenesis of septic cardiomyopathy mainly focuses on two aspects: the systemic neuroimmune mechanism and the local changes of cardiomyocytes. The former mainly includes the autonomic nervous dysfunction mainly caused by sympathetic overactivation and the inflammatory storm induced by immune response disorder. The latter covers the dysregulation of calcium homeostasis, mitochondrial dysfunction and energy metabolism disorder of cardiomyocytes. Immune dysfunction is one of the key factors that cause the poor prognosis of patients with septic cardiomyopathy. Macrophages are sentinel cells of the body's innate immunity. Cardiac macrophages have been confirmed to be one of the most heterogeneous immune cells in the heart. According to their origin and differentiation, they can be divided into bone marrow-derived tissue infiltrating macrophages and cardiac resident macrophages, which have roles of polarization, phagocytosis, regulation of inflammatory response, and participate in innate and adaptive immunity. In the occurrence and development of septic cardiomyopathy, cardiac macrophages recruited from the blood participate in balancing the inflammation and repair of myocardial tissue through the conversion of pro-inflammatory phenotype and anti-inflammatory phenotype. Cardiac resident macrophages mediate immune phagocytosis to maintain the local homeostasis of cardiomyocytes, and the glycometabolic reprogramming of macrophages regulates the release of inflammatory factors, while macrophage metabolic reprogramming regulates the release of inflammatory factors. A deeper understanding of the biological behavior of macrophages, and regulating the polarization, metabolism and phagocytosis of cardiac macrophages, could serve as new target for the prevention and treatment of septic cardiomyopathy. Therefore, this article reviews the key pathogenesis of septic cardiomyopathy and the role of macrophages of different origins and differentiation, revealing the possibility of developing new strategies for the prevention and treatment of septic cardiomyopathy.

巨噬细胞在脓毒性心肌病发病机制中的作用
败血症是一种危及生命的器官功能障碍,由身体对感染的失调反应引起。败血症引起的可逆性心肌功能障碍被称为感染性心肌病。深入了解脓毒症心肌病的发病机制,对早期干预预防其发展,提高脓毒症治疗成功率至关重要。目前,对脓毒性心肌病发病机制的研究主要集中在系统性神经免疫机制和心肌细胞局部改变两个方面。前者主要包括交感神经过度激活引起的自主神经功能障碍和免疫反应紊乱引起的炎症风暴。后者包括心肌细胞钙稳态失调、线粒体功能障碍和能量代谢紊乱。免疫功能障碍是导致脓毒性心肌病患者预后不良的关键因素之一。巨噬细胞是机体先天免疫的前哨细胞。心脏巨噬细胞已被证实是心脏中最异质的免疫细胞之一。根据其来源和分化,可分为骨髓源性组织浸润性巨噬细胞和心脏常驻性巨噬细胞,具有极化、吞噬、调节炎症反应、参与先天免疫和适应性免疫等作用。在脓毒性心肌病的发生发展过程中,从血液中募集的心脏巨噬细胞通过促炎表型和抗炎表型的转化,参与心肌组织的炎症平衡和修复。心脏常驻巨噬细胞介导免疫吞噬维持心肌细胞局部稳态,巨噬细胞糖代谢重编程调节炎症因子的释放,巨噬细胞代谢重编程调节炎症因子的释放。深入了解巨噬细胞的生物学行为,调控心脏巨噬细胞的极化、代谢和吞噬作用,可作为防治脓毒性心肌病的新靶点。因此,本文综述了脓毒性心肌病的关键发病机制以及不同来源和分化的巨噬细胞的作用,揭示了开发预防和治疗脓毒性心肌病新策略的可能性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Zhonghua wei zhong bing ji jiu yi xue
Zhonghua wei zhong bing ji jiu yi xue Medicine-Critical Care and Intensive Care Medicine
CiteScore
1.00
自引率
0.00%
发文量
42
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信