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| Item Type: | Article |
|---|---|
| Title: | Cardiac myocyte miR-29 promotes pathological remodeling of the heart by activating Wnt signaling |
| Creators Name: | Sassi, Y., Avramopoulos, P., Ramanujam, D., Grüter, L., Werfel, S., Giosele, S., Brunner, A.D., Esfandyari, D., Papadopoulou, A.S, De Strooper, B., Hübner, N., Kumarswamy, R., Thum, T., Yin, X., Mayr, M., Laggerbauer, B. and Engelhardt, S. |
| Abstract: | Chronic cardiac stress induces pathologic hypertrophy and fibrosis of the myocardium. The microRNA-29 (miR-29) family has been found to prevent excess collagen expression in various organs, particularly through its function in fibroblasts. Here, we show that miR-29 promotes pathologic hypertrophy of cardiac myocytes and overall cardiac dysfunction. In a mouse model of cardiac pressure overload, global genetic deletion of miR-29 or antimiR-29 infusion prevents cardiac hypertrophy and fibrosis and improves cardiac function. Targeted deletion of miR-29 in cardiac myocytes in vivo also prevents cardiac hypertrophy and fibrosis, indicating that the function of miR-29 in cardiac myocytes dominates over that in non-myocyte cell types. Mechanistically, we found cardiac myocyte miR-29 to de-repress Wnt signaling by directly targeting four pathway factors. Our data suggests that, cell- or tissue-specific antimiR-29 delivery may have therapeutic value for pathological cardiac remodeling and fibrosis. |
| Keywords: | Cardiac Myocytes, Cardiomegaly, Inbred C57BL Mice, Knockout Mice, MicroRNAs, Myocardium, Signal Transduction, Wnt Proteins, Animals, Mice |
| Source: | Nature Communications |
| ISSN: | 2041-1723 |
| Publisher: | Nature Publishing Group |
| Volume: | 8 |
| Number: | 1 |
| Page Range: | 1614 |
| Date: | 20 November 2017 |
| Official Publication: | https://doi.org/10.1038/s41467-017-01737-4 |
| PubMed: | View item in PubMed |
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