The E3 ubiquitin ligase HectD3 attenuates cardiac hypertrophy and inflammation in mice
Myocardial inflammation has recently been recognized as a distinct feature of cardiac hypertrophy and heart failure. HectD3, a HECT domain containing E3 ubiquitin ligase has previously been investigated in the host defense against infections as well as neuroinflammation; its cardiac function however...
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| Hauptverfasser: | , , , , , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
09 October 2020
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| In: |
Communications biology
Year: 2020, Jahrgang: 3, Pages: 1-15 |
| ISSN: | 2399-3642 |
| DOI: | 10.1038/s42003-020-01289-2 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/s42003-020-01289-2 Verlag, lizenzpflichtig, Volltext: https://www.nature.com/articles/s42003-020-01289-2 
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| Verfasserangaben: | Ashraf Yusuf Rangrez, Ankush Borlepawar, Nesrin Schmiedel, Anushka Deshpande, Anca Remes, Manju Kumari, Alexander Bernt, Lynn Christen, Andreas Helbig, Andreas Jungmann, Samuel Sossalla, Andreas Tholey, Oliver J. Müller, Derk Frank & Norbert Frey |
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| 245 | 1 | 4 | |a The E3 ubiquitin ligase HectD3 attenuates cardiac hypertrophy and inflammation in mice |c Ashraf Yusuf Rangrez, Ankush Borlepawar, Nesrin Schmiedel, Anushka Deshpande, Anca Remes, Manju Kumari, Alexander Bernt, Lynn Christen, Andreas Helbig, Andreas Jungmann, Samuel Sossalla, Andreas Tholey, Oliver J. Müller, Derk Frank & Norbert Frey |
| 246 | 3 | 3 | |a The E three ubiquitin ligase HectD three attenuates cardiac hypertrophy and inflammation in mice |
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| 520 | |a Myocardial inflammation has recently been recognized as a distinct feature of cardiac hypertrophy and heart failure. HectD3, a HECT domain containing E3 ubiquitin ligase has previously been investigated in the host defense against infections as well as neuroinflammation; its cardiac function however is still unknown. Here we show that HectD3 simultaneously attenuates Calcineurin-NFAT driven cardiomyocyte hypertrophy and the pro-inflammatory actions of LPS/interferon-γ via its cardiac substrates SUMO2 and Stat1, respectively. AAV9-mediated overexpression of HectD3 in mice in vivo not only reduced cardiac SUMO2/Stat1 levels and pathological hypertrophy but also largely abolished macrophage infiltration and fibrosis induced by pressure overload. Taken together, we describe a novel cardioprotective mechanism involving the ubiquitin ligase HectD3, which links anti-hypertrophic and anti-inflammatory effects via dual regulation of SUMO2 and Stat1. In a broader perspective, these findings support the notion that cardiomyocyte growth and inflammation are more intertwined than previously anticipated. | ||
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