Macrophage Polarization, Metabolic Reprogramming, and Inflammatory Effects in Ischemic Heart Disease.

IF 5.9 2区 医学 Q1 IMMUNOLOGY Frontiers in Immunology Pub Date : 2022-07-18 eCollection Date: 2022-01-01 DOI:10.3389/fimmu.2022.934040
Xiaoqian Sun, Yanqin Li, Qiong Deng, Yueyao Hu, Jianteng Dong, Wei Wang, Yong Wang, Chun Li
{"title":"Macrophage Polarization, Metabolic Reprogramming, and Inflammatory Effects in Ischemic Heart Disease.","authors":"Xiaoqian Sun,&nbsp;Yanqin Li,&nbsp;Qiong Deng,&nbsp;Yueyao Hu,&nbsp;Jianteng Dong,&nbsp;Wei Wang,&nbsp;Yong Wang,&nbsp;Chun Li","doi":"10.3389/fimmu.2022.934040","DOIUrl":null,"url":null,"abstract":"<p><p>Macrophages are highly plastic cells, and the polarization-activating actions that represent their functional focus are closely related to metabolic reprogramming. The metabolic reprogramming of macrophages manifests itself as a bias toward energy utilization, transforming their inflammatory phenotype by changing how they use energy. Metabolic reprogramming effects crosstalk with the biological processes of inflammatory action and are key to the inflammatory function of macrophages. In ischemic heart disease, phenotypic polarization and metabolic shifts in circulating recruitment and tissue-resident macrophages can influence the balance of inflammatory effects in the heart and determine disease regression and prognosis. In this review, we present the intrinsic link between macrophage polarization and metabolic reprogramming, discussing the factors that regulate macrophages in the inflammatory effects of ischemic heart disease. Our aim is to estabilsh reliable regulatory pathways that will allow us to better target the macrophage metabolic reprogramming process and improve the symptoms of ischemic heart disease.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":" ","pages":"934040"},"PeriodicalIF":5.9000,"publicationDate":"2022-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9339672/pdf/","citationCount":"5","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers in Immunology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3389/fimmu.2022.934040","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2022/1/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 5

Abstract

Macrophages are highly plastic cells, and the polarization-activating actions that represent their functional focus are closely related to metabolic reprogramming. The metabolic reprogramming of macrophages manifests itself as a bias toward energy utilization, transforming their inflammatory phenotype by changing how they use energy. Metabolic reprogramming effects crosstalk with the biological processes of inflammatory action and are key to the inflammatory function of macrophages. In ischemic heart disease, phenotypic polarization and metabolic shifts in circulating recruitment and tissue-resident macrophages can influence the balance of inflammatory effects in the heart and determine disease regression and prognosis. In this review, we present the intrinsic link between macrophage polarization and metabolic reprogramming, discussing the factors that regulate macrophages in the inflammatory effects of ischemic heart disease. Our aim is to estabilsh reliable regulatory pathways that will allow us to better target the macrophage metabolic reprogramming process and improve the symptoms of ischemic heart disease.

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
巨噬细胞极化、代谢重编程和缺血性心脏病的炎症作用。
巨噬细胞是高度可塑性的细胞,代表其功能焦点的极化激活行为与代谢重编程密切相关。巨噬细胞的代谢重编程表现为对能量利用的偏好,通过改变它们使用能量的方式来改变它们的炎症表型。代谢重编程效应与炎症作用的生物学过程相互作用,是巨噬细胞炎症功能的关键。在缺血性心脏病中,循环募集和组织驻留巨噬细胞的表型极化和代谢变化可以影响心脏炎症作用的平衡,并决定疾病的消退和预后。在这篇综述中,我们提出巨噬细胞极化与代谢重编程之间的内在联系,讨论了在缺血性心脏病炎症作用中调节巨噬细胞的因素。我们的目标是建立可靠的调控途径,使我们能够更好地靶向巨噬细胞代谢重编程过程,改善缺血性心脏病的症状。
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 去求助
来源期刊
CiteScore
9.80
自引率
11.00%
发文量
7153
审稿时长
14 weeks
期刊介绍: Frontiers in Immunology is a leading journal in its field, publishing rigorously peer-reviewed research across basic, translational and clinical immunology. This multidisciplinary open-access journal is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians and the public worldwide. Frontiers in Immunology is the official Journal of the International Union of Immunological Societies (IUIS). Encompassing the entire field of Immunology, this journal welcomes papers that investigate basic mechanisms of immune system development and function, with a particular emphasis given to the description of the clinical and immunological phenotype of human immune disorders, and on the definition of their molecular basis.
期刊最新文献
POLB 001, a p38 MAPK inhibitor, decreases local and systemic inflammatory responses following in vivo LPS administration in healthy volunteers: a randomised, double-blind, placebo-controlled study. Positive B cell flow cytometry crossmatch without detectable donor-specific antibodies: true or false reactivity? MYC at the tumor-immune interface: mechanisms of immune escape and immunotherapy resistance. New insights into the tumor immune microenvironment and immunotherapy of thyroid cancer. Single-cell transcriptomics reveals keratinocyte dynamic processes associated with S100a4 expression in psoriasiform dermatitis.
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1