In support of this, neutrophil-depleted mice have increased microphage proliferation at the myocardial infarct site but lower expression of MERTK in macrophages (a phagocytosis receptor) with decreased clearance of apoptotic cardiomyocytes, phenotypically manifesting as worse cardiac function post-infarct with increased fibrosis, whereas MERTK expression could be restored in vitro in the presence of NGAL [171]. Here, LCN2 is linked to myocardial infarction.