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| Content Provider | PubMed Central |
|---|---|
| Author | Feng, Ning Huke, Sabine Zhu, Guangshuo Tocchetti, Carlo G. Shi, Sa Aiba, Takeshi Nina, Kaludercic Hoover, Donald B. Beck, Sarah E. Mankowski, Joseph L. Tomaselli, Gordon F. Bers, Donald M. Kass, David A. Nazareno, Paolocci |
| Abstract | BDNF plays a key role in neuron development, survival, and function, with actions occurring through the stimulation of the tropomyosin-related kinase receptor B (TrkB) receptor. Whether BDNF/TrkB signaling has any physiologic role in governing myocardial function is unknown. Here we report that intact BDNF/TrkB signaling is required for the heart to fully contract and relax. These actions occur independently from and in addition to β-adrenergic influence. BDNF-induced enhancement of myocardial performance occurs via direct modulation of Ca2+ cycling in a calmodulin-dependent protein kinase II-dependent manner. Thus, BDNF/TrkB signaling represents a previously unidentified way by which the peripheral nervous system controls cardiac muscle physiology. Our study suggests that loss or alterations in BDNF/TrkB stimulation may contribute to the pathogenesis of myocardial dysfunction in acute or chronic disease conditions. |
| Related Links | http://dx.doi.org/10.1073/pnas.1417949112 |
| Ending Page | 1885 |
| Page Count | 6 |
| Starting Page | 1880 |
| File Format | |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 6 |
| Volume Number | 112 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2015-02-10 |
| Access Restriction | Open |
| Rights Holder | National Academy of Sciences |
| Subject Keyword | General Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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