Why the study?
Although miR155 is upregulated after myocardial infarction and regulates remodeling via inflammation, fibrosis, and cardiomyocyte hypertrophy, its role in cardiac remodeling and dysfunction in dyslipidemia remained unclear.
Does miR155 deficiency improve cardiac function and remodeling after myocardial infarction in a dyslipidemic mouse model?
Does miR155 deficiency improve cardiac function and remodeling after myocardial infarction in a dyslipidemic mouse model?
In a dyslipidemic mouse model of myocardial infarction, miR155 deficiency reduces myofibroblast density but does not improve cardiac function or reduce infarct size.
miR-155 depletion reduces post-MI myofibroblast density without functional benefit in dyslipidemic mice; leaves open therapeutic relevance in humans.
Myocardial infarction remains the most common cause of heart failure with adverse remodeling. MicroRNA (miR)155 is upregulated following myocardial infarction and represents a relevant regulatory factor for cardiac remodeling by engagement in cardiac inflammation, fibrosis and cardiomyocyte hypertrophy. Here, we investigated the role of miR155 in cardiac remodeling and dysfunction following myocardial infarction in a dyslipidemic mouse model. Myocardial infarction was induced in dyslipidemic apolipoprotein E-deficient (ApoE−/−) mice with and without additional miR155 knockout by ligation of the LAD. Four weeks later, echocardiography was performed to assess left ventricular (LV) dimensions and function, and mice were subsequently sacrificed for histological analysis. Echocardiography revealed no difference in LV ejection fractions, LV mass and LV volumes between ApoE−/− and ApoE−/−/miR155−/− mice. Histology confirmed comparable infarction size and unaltered neoangiogenesis in the myocardial scar. Notably, myofibroblast density was significantly decreased in ApoE−/−/miR155−/− mice compared to the control, but no difference was observed for total collagen deposition. Our findings reveal that genetic depletion of miR155 in a dyslipidemic mouse model of myocardial infarction does not reduce infarction size and consecutive heart failure but does decrease myofibroblast density in the post-ischemic scar.
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Schumacher et al. (2021) studied this question.
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