Motivation: Multiple cardiac and non-cardiac cell types are involved in the remodelling process after myocardial infarction. Insulin-like growth factor 1 (IGF1) preserves cardiac function after myocardial infarction. However, it is unknown whether the beneficial effect of IGF1 is mediated by IGF1 receptor (IGF1R) signalling in cardiomyocytes. Methods: All experiments were performed after approval of the local animal ethics committee. Two independent experimental series were conducted: In series 1, C57BL/6 mice were investigated, and in series 2, IGF1R flox/flox mice, which were crossbred with alpha-MHC Cre-deleter mice to achieve a tamoxifen inducible cardiomyocyte specific knock out (iCMIGF1RKO; KO and WT, respectively) were investigated. All mice of both series underwent 45 minutes regional myocardial ischemia followed by four weeks of reperfusion. Regional myocardial ischemia was initiated in anesthetized mice (2% isoflurane; 0.1 mg/kg buprenorphine, s.c.) after lateral thoracotomy by temporary ligation of the left coronary artery. At the onset of reperfusion, mice received either vehicle (Con) or IGF1 as bolus (40 ng/g, i.p.) followed by continuous infusion over three days using osmotic mini pumps (1 µg/g/d, s.c.). Left ventricular function (end diastolic (EDV), end systolic volume (ESV), and ejection fraction (EF)) was analyzed by echocardiography at baseline and week 1 and 4 after I/R. In addition, regional wall motion was analyzed using strain analysis in series 2. Results: No differences in left ventricular function between groups in both series were observed at baseline (EF: series 1; 64±4% (Con), 66±3% (IGF1); series 2; 60±4% (WT-Con), 60±2% (WT-IGF1), 60±5% (KO-Con), 58±2% (KO-IGF1). In C57BL/6 mice (series 1), myocardial infarction caused a moderate left ventricular dilatation shown by an increase in EDV of about 33% (92±17 µl at week 4 vs. 69±10 µl at baseline). IGF1-treatment reduced left ventricular dilatation compared to vehicle treated animals at week 4 (79±13 µl vs. 92±17 µl). This IGF1-effect was accompanied by an improved EF both at week 1 (54±9% vs. 34±5 %) and 4 (49±13% vs. 33±4%). In iCMIGF1RKO (series 2), an improved cardiac function by IGF1 was not only detected in WT mice (EF, week 4: 49±4% (WT-IGF1) vs. 36±8% (WT-Con)), but also in KO animals (EF, week 4: 48±5% (KO-IGF1) vs. 35±5% (KO-Con)). Analysis of regional endocardial displacement showed an improved wall motion in the segments that has been ischemic, but had no effect within wall segments that belong to the remote myocardium. Conclusion: Our results clearly demonstrate that short-term IGF1 treatment improves myocardial function after I/R. The preservation of cardiac function might rather be caused by an improved function within the myocardial segments that had been ischemic than by an increased functional compensation within the remote myocardium. Interestingly, the IGF1R in cardiomyocytes is not necessary for the protective IGF1-effect.