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Isolation of Macrophage Subsets and Stromal Cells from Human and Mouse Myocardial Specimens
Published on: December 17, 2019
Crosstalk Between Cardiac Cells and Macrophages Postmyocardial Infarction: Insights from In Vitro Studies
Pamela Hitscherich1, Eun Jung Lee1
1Department of Biomedical Engineering, New Jersey Institute of Technology, Newark, New Jersey, USA.
Insights
Myocardial infarction (MI) triggers complex inflammation. In vitro cardiac models reveal macrophage and cardiac cell interactions, offering insights into repair and potential new treatments.
Area of Science:
- Cardiovascular research
- Immunology
- Regenerative medicine
Background:
- Cardiovascular disease, particularly myocardial infarction (MI), is a leading cause of mortality.
- Post-MI, cardiomyocyte loss and inflammatory cell infiltration, including macrophages, are critical.
- The precise role of macrophage subsets in cardiac cell function and survival post-MI remains unclear.
Purpose of the Study:
- To review existing in vitro cardiac disease models.
- To examine macrophage and cardiac cell interactions post-MI.
- To discuss challenges and future directions for in vitro cardiac models.
Main Methods:
- Literature review of studies utilizing in vitro cardiac models.
- Analysis of interactions between macrophages and cardiomyocytes, endothelial cells, and fibroblasts.
- Discussion of mechanistic insights into the inflammatory cascade post-MI.
Main Results:
- In vitro models are crucial for understanding the complex inflammatory cascade post-MI.
- These models facilitate the study of interactions between macrophages and various cardiac cell types.
- Insights into multicellular interactions post-MI are provided by these models.
Conclusions:
- In vitro cardiac models bridge a critical gap in understanding post-MI inflammation.
- Mechanistic insights into macrophage-cardiac cell interactions can drive therapeutic and diagnostic advancements.
- Further development of these models holds promise for revolutionizing cardiovascular disease treatment.
Abstract:
Cardiovascular disease, including myocardial infarction (MI), is the leading cause of death in the western world. Following MI, a large number of cardiomyocytes are lost and inflammatory cells such as monocytes and macrophages migrate into the damaged region to remove dead cells and tissue. These inflammatory cells secrete growth factors to induce degradation of the extracellular matrix in the myocardium and recruit cardiac fibroblasts. However, the contribution of specific macrophage subsets on cardiac cell function and survival in the steady state as well as in the diseased state is not well known. There is an increasing demand for in vitro cardiac disease models to bridge the critical missing link in the existing experimental methods. In this review, studies using in vitro models to examine the interaction between macrophages and cardiac cells, including cardiomyocytes, endothelial cells, and fibroblasts, are summarized to better understand the complex inflammatory cascade post-MI. The current challenges and the future directions of in vitro cardiac models are also discussed. Detailed and more mechanistic insights into macrophages and cardiac cell interactions during the multiphase repair process could potentially revolutionize the development of treatments and diagnostic alternatives. Impact statement The inflammatory cascade postmyocardial infarction (MI) is very complex. In vitro cardiac disease model studies bridge the critical missing link in the existing experimental methods and provide insights, including multicellular interaction post-MI. Detailed and more mechanistic insights into macrophages and cardiac cell interactions during the multiphase repair process could potentially revolutionize in developing treatments and diagnostic alternatives.
