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Updated: Nov 8, 2025
Isolation of Macrophage Subsets and Stromal Cells from Human and Mouse Myocardial Specimens
Published on: December 17, 2019
New Insights and Novel Therapeutic Potentials for Macrophages in Myocardial Infarction
Zenglei Zhang1,2, Junnan Tang3,4, Xiaolin Cui5
1Department of Cardiology, First Affiliated Hospital of Zhengzhou University, NO. 1 Eastern Jianshe Road, Zhengzhou, 450052, Henan, China.
Insights
Macrophages are key immune cells in heart attack (myocardial infarction) development and progression. Understanding their roles in inflammation and repair offers new therapeutic strategies for cardiovascular disease.
Area of Science:
- Immunology
- Cardiology
- Pathophysiology
Background:
- Cardiovascular disease (CVD), particularly myocardial infarction (MI), remains a leading global cause of mortality.
- Inflammation is increasingly recognized as a critical factor in the pathogenesis of atherosclerosis and CVD.
- Macrophages, crucial innate immune cells, are pivotal in the initiation and progression of atherosclerosis.
Purpose of the Study:
- To review the multifaceted roles of macrophages in myocardial infarction (MI) development and progression.
- To explore factors that regulate macrophage activation and function within the cardiac environment.
- To discuss the therapeutic potential of targeting macrophages in MI, including nanoparticle-mediated drug delivery.
Main Methods:
- Literature review focusing on the role of macrophages in cardiovascular disease and myocardial infarction.
- Analysis of studies investigating macrophage phenotypes (M1 and M2) in cardiac injury and repair.
- Examination of research on macrophage-based therapeutic strategies for MI.
Main Results:
- Cardiac macrophage populations expand significantly following injury, such as MI.
- Classically activated macrophages (M1) drive initial cardiac remodeling post-MI, while alternatively activated macrophages (M2) promote subsequent repair.
- Macrophages are implicated in both the detrimental inflammatory phase and the beneficial repair phase of MI.
Conclusions:
- Macrophages are central players in the inflammatory and reparative processes following myocardial infarction.
- Modulating macrophage activation and function presents a promising therapeutic avenue for managing MI and CVD.
- Nanoparticle-based drug delivery systems targeting macrophages offer potential for innovative MI treatments.
Abstract:
Cardiovascular disease (CVD) has long been the leading cause of death worldwide, and myocardial infarction (MI) accounts for the greatest proportion of CVD. Recent research has revealed that inflammation plays a major role in the pathogenesis of CVD and other manifestations of atherosclerosis. Overwhelming evidence supports the view that macrophages, as the basic cell component of the innate immune system, play a pivotal role in atherosclerosis initiation and progression. Limited but indispensable resident macrophages have been detected in the healthy heart; however, the number of cardiac macrophages significantly increases during cardiac injury. In the early period of initial cardiac damage (e.g., MI), numerous classically activated macrophages (M1) originating from the bone marrow and spleen are rapidly recruited to damaged sites, where they are responsible for cardiac remodeling. After the inflammatory stage, the macrophages shift toward an alternatively activated phenotype (M2) that promotes cardiac repair. In addition, extensive studies have shown the therapeutic potential of macrophages as targets, especially for emerging nanoparticle-mediated drug delivery systems. In the present review, we focused on the role of macrophages in the development and progression of MI, factors regulating macrophage activation and function, and the therapeutic potential of macrophages in MI.
