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| 001 | 132443 | ||
| 005 | 20240229111722.0 | ||
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| 100 | 1 | _ | |a Lehmann, Lorenz H |b 0 |
| 245 | _ | _ | |a A proteolytic fragment of histone deacetylase 4 protects the heart from failure by regulating the hexosamine biosynthetic pathway. |
| 260 | _ | _ | |a New York, NY |c 2018 |b Nature America Inc. |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1550485774_632 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
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| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a The stress-responsive epigenetic repressor histone deacetylase 4 (HDAC4) regulates cardiac gene expression. Here we show that the levels of an N-terminal proteolytically derived fragment of HDAC4, termed HDAC4-NT, are lower in failing mouse hearts than in healthy control hearts. Virus-mediated transfer of the portion of the Hdac4 gene encoding HDAC4-NT into the mouse myocardium protected the heart from remodeling and failure; this was associated with decreased expression of Nr4a1, which encodes a nuclear orphan receptor, and decreased NR4A1-dependent activation of the hexosamine biosynthetic pathway (HBP). Conversely, exercise enhanced HDAC4-NT levels, and mice with a cardiomyocyte-specific deletion of Hdac4 show reduced exercise capacity, which was characterized by cardiac fatigue and increased expression of Nr4a1. Mechanistically, we found that NR4A1 negatively regulated contractile function in a manner that depended on the HBP and the calcium sensor STIM1. Our work describes a new regulatory axis in which epigenetic regulation of a metabolic pathway affects calcium handling. Activation of this axis during intermittent physiological stress promotes cardiac function, whereas its impairment in sustained pathological cardiac stress leads to heart failure. |
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| 700 | 1 | _ | |a Jebessa, Zegeye H |b 1 |
| 700 | 1 | _ | |a Kreusser, Michael M |b 2 |
| 700 | 1 | _ | |a Horsch, Axel |b 3 |
| 700 | 1 | _ | |a He, Tao |b 4 |
| 700 | 1 | _ | |a Kronlage, Mariya |b 5 |
| 700 | 1 | _ | |a Dewenter, Matthias |b 6 |
| 700 | 1 | _ | |a Sramek, Viviana |b 7 |
| 700 | 1 | _ | |a Oehl, Ulrike |b 8 |
| 700 | 1 | _ | |a Krebs-Haupenthal, Jutta |b 9 |
| 700 | 1 | _ | |a von der Lieth, Albert H |b 10 |
| 700 | 1 | _ | |a Schmidt, Andrea |b 11 |
| 700 | 1 | _ | |a Sun, Qiang |b 12 |
| 700 | 1 | _ | |a Ritterhoff, Julia |b 13 |
| 700 | 1 | _ | |a Finke, Daniel |b 14 |
| 700 | 1 | _ | |a Völkers, Mirko |b 15 |
| 700 | 1 | _ | |a Jungmann, Andreas |b 16 |
| 700 | 1 | _ | |a Sauer, Sven W |b 17 |
| 700 | 1 | _ | |a Thiel, Christian |b 18 |
| 700 | 1 | _ | |a Nickel, Alexander |b 19 |
| 700 | 1 | _ | |a Kohlhaas, Michael |b 20 |
| 700 | 1 | _ | |a Schäfer, Michaela |b 21 |
| 700 | 1 | _ | |a Sticht, Carsten |b 22 |
| 700 | 1 | _ | |a Maack, Christoph |b 23 |
| 700 | 1 | _ | |a Gretz, Norbert |b 24 |
| 700 | 1 | _ | |a Wagner, Michael |b 25 |
| 700 | 1 | _ | |a El-Armouche, Ali |b 26 |
| 700 | 1 | _ | |a Maier, Lars S |b 27 |
| 700 | 1 | _ | |a Londoño, Juan E Camacho |b 28 |
| 700 | 1 | _ | |a Meder, Benjamin |b 29 |
| 700 | 1 | _ | |a Freichel, Marc |b 30 |
| 700 | 1 | _ | |a Gröne, Hermann-Josef |0 P:(DE-He78)00a2ea610aee4a8fca32908fc3d02e91 |b 31 |u dkfz |
| 700 | 1 | _ | |a Most, Patrick |b 32 |
| 700 | 1 | _ | |a Müller, Oliver J |0 0000-0001-8223-2638 |b 33 |
| 700 | 1 | _ | |a Herzig, Stephan |0 P:(DE-He78)e527f794b23172e769c8904180546f57 |b 34 |u dkfz |
| 700 | 1 | _ | |a Furlong, Eileen E M |0 0000-0002-9544-8339 |b 35 |
| 700 | 1 | _ | |a Katus, Hugo A |b 36 |
| 700 | 1 | _ | |a Backs, Johannes |0 0000-0002-2322-2699 |b 37 |
| 773 | _ | _ | |a 10.1038/nm.4452 |g Vol. 24, no. 1, p. 62 - 72 |0 PERI:(DE-600)1484517-9 |n 1 |p 62 - 72 |t Nature medicine |v 24 |y 2018 |x 1546-170X |
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