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| Home > Publications database > Various effects of AAV9-mediated βARKct gene therapy on the heart in dystrophin-deficient (mdx) mice and δ-sarcoglycan-deficient (Sgcd-/-) mice. > print |
| Home > Publications database > Various effects of AAV9-mediated βARKct gene therapy on the heart in dystrophin-deficient (mdx) mice and δ-sarcoglycan-deficient (Sgcd-/-) mice. > print |
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| 100 | 1 | _ | |a Bauer, Ralf |b 0 |
| 245 | _ | _ | |a Various effects of AAV9-mediated βARKct gene therapy on the heart in dystrophin-deficient (mdx) mice and δ-sarcoglycan-deficient (Sgcd-/-) mice. |
| 260 | _ | _ | |a Amsterdam [u.a.] |c 2019 |b Elsevier Science |
| 336 | 7 | _ | |a article |2 DRIVER |
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| 520 | _ | _ | |a So far effective strategies to treat cardiomyopathy in patients with muscular dystrophies are still not clearly defined. Previously, treatment with β-blockers showed beneficial effects on the development of cardiomyopathy in dystrophin-deficient (mdx) mice, but not in δ-sarcoglycan-deficient (Sgcd-/-) mice. We therefore aimed to study a more specific approach to target maladaptive β-adrenergic signalling in these mice. It has been shown that lowering cardiac G-protein-coupled-receptor-kinase-2 (GRK2) activity with βARKct expression, a peptide inhibitor of protein-coupled-receptor-kinase-2 (GRK2), results in improvement of heart failure in several different animal models. We therefore investigated whether adeno-associated virus type 9 (AAV9)-mediated gene delivery of βARKct, could ameliorate cardiac pathology in mdx and Sgcd-/- mice. We found that long-term treatment with AAV9- βARKct-cDNA with a cardiac-specific promoter significantly improves left ventricular systolic function and reduces myocardial hypertrophy in mdx mice, whereas only mild beneficial effects on cardiac function is observed in Sgcd-/- mice. Interestingly, in contrast to mdx mice neither GRK2 nor nuclear-factor-kappaB (NFκB) were upregulated in Sgcd-/- mice. Taken together, effectiveness of AAV-mediated βARKct therapy may vary between different genetic mutations and presumably depend on the state of adrenergic dysregulation mediated through the upregulation of GRK2. |
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| 700 | 1 | _ | |a Enns, Helene |b 1 |
| 700 | 1 | _ | |a Jungmann, Andreas |b 2 |
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| 700 | 1 | _ | |a Volz, Christian |b 4 |
| 700 | 1 | _ | |a Schinkel, Stefanie |b 5 |
| 700 | 1 | _ | |a Koch, Walter J |b 6 |
| 700 | 1 | _ | |a Raake, Philip W |b 7 |
| 700 | 1 | _ | |a Most, Patrick |b 8 |
| 700 | 1 | _ | |a Katus, Hugo A |b 9 |
| 700 | 1 | _ | |a Müller, Oliver J |b 10 |
| 773 | _ | _ | |a 10.1016/j.nmd.2018.12.006 |g Vol. 29, no. 3, p. 231 - 241 |0 PERI:(DE-600)2008287-3 |n 3 |p 231 - 241 |t Neuromuscular disorders |v 29 |y 2019 |x 0960-8966 |
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