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.