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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. and Avramopoulos, P. and Ramanujam, D. and Grüter, L. and Werfel, S. and Giosele, S. and Brunner, A.D. and Esfandyari, D. and Papadopoulou, A.S and De Strooper, B. and Hübner, N. and Kumarswamy, R. and Thum, T. and Yin, X. and Mayr, M. and 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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