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Project A06 (Gödecke)

Mechanism of IGF1-dependent modulation of myeloid cell function and metabolism in acute myocardial infarction

We have shown previously that short-term IGF1 treatment after acute myocardial infarction reduces scar size, enhances angiogenesis, and improves cardiac function via modulation of myeloid cells. In the next period the project aims at i) identification of the cell type being responsible for this effect (macrophages, neutrophils), ii) elucidation of the molecular alterations induced by IGF1 in these cells, and iii) investigation of the IGF1-mediated cardioprotection in the context of insulin resistance/ T2DM as a relevant comorbidity in AMI. In summary, the project will identify novel mechanisms of immune cell modulation which improve the outcome after AMI.

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