Search citation statements
Paper Sections
Citation Types
Year Published
Publication Types
Relationship
Authors
Journals
The immune response holds a pivotal role in cardiovascular disease development. As multifunctional cells of the innate immune system, macrophages play an essential role in initial inflammatory response that occurs following cardiovascular injury, thereby inducing subsequent damage while also facilitating recovery. Meanwhile, the diverse phenotypes and phenotypic alterations of macrophages strongly associate with distinct types and severity of cardiovascular diseases, including coronary heart disease, valvular disease, myocarditis, cardiomyopathy, heart failure, atherosclerosis and aneurysm, which underscores the importance of investigating macrophage regulatory mechanisms within the context of specific diseases. Besides, recent strides in single-cell sequencing technologies have revealed macrophage heterogeneity, cell–cell interactions, and downstream mechanisms of therapeutic targets at a higher resolution, which brings new perspectives into macrophage-mediated mechanisms and potential therapeutic targets in cardiovascular diseases. Remarkably, myocardial fibrosis, a prevalent characteristic in most cardiac diseases, remains a formidable clinical challenge, necessitating a profound investigation into the impact of macrophages on myocardial fibrosis within the context of cardiac diseases. In this review, we systematically summarize the diverse phenotypic and functional plasticity of macrophages in regulatory mechanisms of cardiovascular diseases and unprecedented insights introduced by single-cell sequencing technologies, with a focus on different causes and characteristics of diseases, especially the relationship between inflammation and fibrosis in cardiac diseases (myocardial infarction, pressure overload, myocarditis, dilated cardiomyopathy, diabetic cardiomyopathy and cardiac aging) and the relationship between inflammation and vascular injury in vascular diseases (atherosclerosis and aneurysm). Finally, we also highlight the preclinical/clinical macrophage targeting strategies and translational implications.
The immune response holds a pivotal role in cardiovascular disease development. As multifunctional cells of the innate immune system, macrophages play an essential role in initial inflammatory response that occurs following cardiovascular injury, thereby inducing subsequent damage while also facilitating recovery. Meanwhile, the diverse phenotypes and phenotypic alterations of macrophages strongly associate with distinct types and severity of cardiovascular diseases, including coronary heart disease, valvular disease, myocarditis, cardiomyopathy, heart failure, atherosclerosis and aneurysm, which underscores the importance of investigating macrophage regulatory mechanisms within the context of specific diseases. Besides, recent strides in single-cell sequencing technologies have revealed macrophage heterogeneity, cell–cell interactions, and downstream mechanisms of therapeutic targets at a higher resolution, which brings new perspectives into macrophage-mediated mechanisms and potential therapeutic targets in cardiovascular diseases. Remarkably, myocardial fibrosis, a prevalent characteristic in most cardiac diseases, remains a formidable clinical challenge, necessitating a profound investigation into the impact of macrophages on myocardial fibrosis within the context of cardiac diseases. In this review, we systematically summarize the diverse phenotypic and functional plasticity of macrophages in regulatory mechanisms of cardiovascular diseases and unprecedented insights introduced by single-cell sequencing technologies, with a focus on different causes and characteristics of diseases, especially the relationship between inflammation and fibrosis in cardiac diseases (myocardial infarction, pressure overload, myocarditis, dilated cardiomyopathy, diabetic cardiomyopathy and cardiac aging) and the relationship between inflammation and vascular injury in vascular diseases (atherosclerosis and aneurysm). Finally, we also highlight the preclinical/clinical macrophage targeting strategies and translational implications.
Objective:To investigate the mechanism of action of Jian-Pi-Qu-Tan Formula in regulating the polarisation balance of M1/M2 type macrophages and attenuating atherosclerosis in ApoE-/-mice. Methods:Ten male SPF-grade C57BL/6J mice were used as the control group (Con group); male SPF-grade ApoE-/- mice, 30 mice, were randomly divided into the AS model group (Mod group), the Jian-Pi-Qu-Tan Formula group (JPQT group), and the atorvastatin calcium tablets group (ATO group) according to the random-number-table method, with 10 mice in each group. Among them, the CON group was given normal feed and the remaining group was given atherosclerotic feed. Gastric administration of drugs was started 8 weeks after modelling, and the corresponding drugs were given by gavage in the JPQT and ATO groups, and an equal amount of saline was given by gavage in the Con and Mod groups for 8 weeks. Body weight was continuously monitored, and after blood collection from the abdominal aorta, the serum TC and TG levels of mice in each group were compared; plaque formation in aortic tissues was observed by HE staining, oil red O staining and Masson staining; the expression levels of pro-inflammatory factors IL-6, IL-12 and anti-inflammatory factor IL-10 were detected by ELISA; and the positive expression of aortic CD86 and CD206 was detected by immunofluorescence; Western blot detected the protein expression levels of aortic iNOS, Arg-1, STAT6 and p-STAT6. Results:Jian-Pi-Qu-Tan Formula significantly improved lipid levels and inflammatory factor levels, attenuated atherosclerotic plaque formation, decreased iNOS protein levels, and increased Arg-1 and p-STAT6 protein levels, and regulated M1/M2 macrophage polarisation in ApoE-/-AS mice. Conclusion:Jian-Pi-Qu-Tan Formula regulates lipid metabolism, reduces inflammation and ameliorates atherosclerosis by activating STAT6 phosphorylation and regulating M1/M2 polarisation balance.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.