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Updated: Jul 12, 2025
Isolation of Macrophage Subsets and Stromal Cells from Human and Mouse Myocardial Specimens
Published on: December 17, 2019
Macrophage-driven cardiac inflammation and healing: insights from homeostasis and myocardial infarction
Wenjie Zuo1, Renhua Sun2, Zhenjun Ji1
1Department of Cardiology, Zhongda Hospital, School of Medicine, Southeast University, No. 87, Dingjiaqiao, Nanjing, 210009, China.
Insights
Myocardial infarction (MI) recovery is complicated by adverse cardiac remodeling. Macrophages are key immune cells influencing this process, but their complex roles go beyond simple M1/M2 classifications, necessitating advanced research for better treatments.
Area of Science:
- Cardiovascular Biology
- Immunology
- Regenerative Medicine
Background:
- Reperfusion therapy improves survival after myocardial infarction (MI), but adverse cardiac remodeling and heart failure remain significant challenges.
- Macrophages are critical in regulating the inflammatory and repair processes post-MI, influencing myocardial injury and remodeling outcomes.
- The classical M1/M2 macrophage polarization model is insufficient for precision medicine, limiting translational research in MI.
Purpose of the Study:
- To review the origins, distribution, classification, and surface markers of macrophages in the context of MI.
- To explore the complex roles of macrophages in cardiac homeostasis and inflammation following myocardial infarction.
- To highlight how advanced technologies like single-cell sequencing reveal macrophage heterogeneity and plasticity for targeted MI interventions.
Main Methods:
- Literature review synthesizing current knowledge on macrophage biology in cardiovascular disease.
- Analysis of recent advances in single-cell sequencing technologies applied to cardiac macrophages.
- Discussion of macrophage origins, tissue distribution, classification, and surface markers relevant to MI.
Main Results:
- Macrophages exhibit significant heterogeneity and plasticity beyond the traditional M1/M2 paradigm.
- Understanding macrophage roles is crucial for mitigating adverse remodeling and preventing heart failure post-MI.
- Single-cell technologies offer unprecedented insights into macrophage functions in the cardiac microenvironment.
Conclusions:
- The simplistic M1/M2 macrophage classification is inadequate for understanding post-MI cardiac repair.
- Targeting macrophage heterogeneity and plasticity holds promise for novel therapeutic strategies after myocardial infarction.
- Further research utilizing advanced sequencing is essential for developing precision medicine approaches for MI patients.
Abstract:
Early and prompt reperfusion therapy has markedly improved the survival rates among patients enduring myocardial infarction (MI). Nonetheless, the resulting adverse remodeling and the subsequent onset of heart failure remain formidable clinical management challenges and represent a primary cause of disability in MI patients worldwide. Macrophages play a crucial role in immune system regulation and wield a profound influence over the inflammatory repair process following MI, thereby dictating the degree of myocardial injury and the subsequent pathological remodeling. Despite numerous previous biological studies that established the classical polarization model for macrophages, classifying them as either M1 pro-inflammatory or M2 pro-reparative macrophages, this simplistic categorization falls short of meeting the precision medicine standards, hindering the translational advancement of clinical research. Recently, advances in single-cell sequencing technology have facilitated a more profound exploration of macrophage heterogeneity and plasticity, opening avenues for the development of targeted interventions to address macrophage-related factors in the aftermath of MI. In this review, we provide a summary of macrophage origins, tissue distribution, classification, and surface markers. Furthermore, we delve into the multifaceted roles of macrophages in maintaining cardiac homeostasis and regulating inflammation during the post-MI period.
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