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August 2017


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The cardiac microenvironment uses non‐canonical WNT signaling to activate monocytes after myocardial infarction. EMBO Molecular Medicine (2017) e201707565, DOI 10.15252/emmm.201707565, DZHK authors: Meyer, Dieterich, Haas, Müller, Boutros, Katus, Leuschner

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Researchers from the DZHK partner site Heidelberg/Mannheim report in EMBO Molecular Medicine about a novel mechanism of monocyte activation following myocardial infarction. Myocytes play a central role in the inflammatory response following coronary circulation disturbances. The researchers examined to what extent the monocytes change during the course of their migration from the point of origin to the site of inflammation. Thus they were able to identify a hitherto unknown mechanism of the Wnt signaling pathway that is crucial for the pro-inflammatory activation of monocytes in the infarct area. In further studies the investigators also succeeded in identifying a regulator molecule (WIF1) of this local activation process. Cardiomyocyte-specific over-expression of WIF1 by means of adeno-associated virus (AAV9) led to a reduction of cardiac inflammation and a significant improvement in left ventricular pump performance. Modulation of the identified mechanism could potentially serve as a therapy to prevent heart failure after myocardial infarction.

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