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Editorial
. 2013 Sep 27;113(8):949-51.
doi: 10.1161/CIRCRESAHA.113.302155.

A MERry response after myocardial infarction

Sanja Arandjelovic  1 , Kodi S Ravichandran
Affiliations
Editorial

A MERry response after myocardial infarction

Sanja Arandjelovic et al. Circ Res. .
No abstract available

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Figures

Figure 1
Figure 1. MER tyrosine kinase deficiency leads to prolonged inflammation after myocardial infarction and increases the size of infarct
Following myocardial infarction, monocytes and macrophages (MF) infiltrate the injury site and clear apoptotic and necrotic cardiomyocytes. Engulfment of apoptotic cells leads to production of anti-inflammatory cytokines by the phagocytes and in turn, dampening further inflammation in the cardiac tissue. In MER deficient mice, clearance of dying cardiomyocytes is delayed, resulting in prolonged inflammation and increased infarct size. After cardiac injury, ADAM17 mediated proteolytic cleavage of MER is thought to result in the appearance of the soluble MER ectodomain (solMER), which might further influence clearance and/or resolution of inflammation in the cardiac tissue.
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References

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