Why the study?
Although macrophages produce factors involved in cardiac repair and remodeling after myocardial infarction, how these factors crosstalk with other cell types mediating repair is not fully understood.
Does selective inactivation of macrophage Mmp14 attenuate cardiac dysfunction and fibrosis after myocardial infarction in a mouse model?
Comparison
MAC-Mmp14 KO vs wild-type counterparts
Authors
Loading...
Macrophage Mmp14 KO attenuates post-MI remodeling in mice; hypothesis-generating and leaves open clinical translation.
Does selective inactivation of macrophage Mmp14 attenuate cardiac dysfunction and fibrosis after myocardial infarction in a mouse model?
Macrophage MT1-MMP is a key regulator of endothelial-to-mesenchymal transition and adverse cardiac remodeling after myocardial infarction.
Alonso-Herranz et al. (2020) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: