TY - JOUR
T1 - Crosstalk between Cardiac Cells and Macrophages Postmyocardial Infarction
T2 - Insights from in Vitro Studies
AU - Hitscherich, Pamela
AU - Lee, Eun Jung
N1 - Funding Information:
This work was supported by the National Institutes of Health [NIH R15 HL145726]; and the National Science Foundation [NSF CAREER 1653464].
Publisher Copyright:
© 2021, Mary Ann Liebert, Inc., publishers.
PY - 2021/10
Y1 - 2021/10
N2 - 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. 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.
AB - 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. 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.
KW - Cardiac cell interaction
KW - Cardiac disease models
KW - Cardiac inflammation
KW - Macrophages
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U2 - 10.1089/ten.teb.2020.0198
DO - 10.1089/ten.teb.2020.0198
M3 - Review article
C2 - 33096955
AN - SCOPUS:85117880310
SN - 1937-3368
VL - 27
SP - 475
EP - 485
JO - Tissue Engineering - Part B: Reviews
JF - Tissue Engineering - Part B: Reviews
IS - 5
ER -