摘要
背景:心肌梗死的特点是心脏血流中断,直接导致全世界范围内的死亡和致残。心脏巨噬细胞表现出明显的特征YPES(如M1或M2)和功能(如促炎或抗炎)对心肌微环境的改变作出反应,并随后加重或消除t的炎症。他心梗。巨噬细胞极化的调节与心肌梗死有关,关系到心脏愈合的质量和结果。 摘要目的:综述目前对心肌梗死巨噬细胞极化调控的认识,突出药物的治疗潜力。调节巨噬细胞极化在心肌损伤治疗中的作用。 结果:及时控制M2/M1比值有助于缓解炎症,促进创面愈合,预防心肌纤维化。右室梗死。 结论:巨噬细胞极化是抗心肌损伤新药的治疗靶点,值得进一步研究。
关键词: 心肌梗死,炎症,巨噬细胞极化,心脏愈合,分子机制,药物发现。
Current Drug Targets
Title:Macrophage Polarization as a Therapeutic Target in Myocardial Infarction
Volume: 19 Issue: 6
关键词: 心肌梗死,炎症,巨噬细胞极化,心脏愈合,分子机制,药物发现。
摘要: Background: Myocardial infarction is characterized by the interruption of blood flow through the heart, directly causing mortality and disability worldwide. Cardiac macrophages exhibit distinct phenotypes (e.g., M1 or M2) and functions (e.g., proinflammatory or anti-inflammatory) in response to the alterations of myocardial microenvironment, and subsequently exacerbate or resolve inflammation in the infarcted hearts. Regulation of macrophage polarization was implicated in myocardial infarction for the quality and outcome of cardiac healing.
Objective: The purpose of this review was to summarise the current understanding on the regulation of macrophage polarization in myocardial infarction and highlight the therapeutic potential of pharmacological regulators in the treatment of myocardial injury via modulating macrophage polarization.
Results: Timely control of M2/M1 ratio by endogenous mediators and pharmacological regulators should help the resolution of inflammation, promote wound healing and prevent cardiac fibrosis after myocardial infarction.
Conclusion: Macrophage polarization deserves better investigations as the therapeutic target for the development of novel drugs against myocardial injury.
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Cite this article as:
Macrophage Polarization as a Therapeutic Target in Myocardial Infarction, Current Drug Targets 2018; 19 (6) . https://dx.doi.org/10.2174/1389450118666171031115025
DOI https://dx.doi.org/10.2174/1389450118666171031115025 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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