AAV-9 mediated phosphatase-1 inhibitor-1 overexpression improves cardiac contractility in unchallenged mice but is deleterious in pressure-overload-Reference-Cited by-同舟云学术

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AAV-9 mediated phosphatase-1 inhibitor-1 overexpression improves cardiac contractility in unchallenged mice but is deleterious in pressure-overload

Published:2018-01 Issue:1 Volume:25 Page:13-19
ISSN:0969-7128
Container-title:Gene Therapy
language:en
Short-container-title:Gene Ther

Author:

Schwab D M,Tilemann L,Bauer R,Heckmann M,Jungmann A,Wagner M,Burgis J,Vettel C,Katus H A,El-Armouche A,Müller O J

Publisher

Springer Science and Business Media LLC

Subject

Genetics,Molecular Biology,Molecular Medicine

Link

http://www.nature.com/articles/gt201797.pdf

Reference16 articles.

1. Neumann J, Eschenhagen T, Jones LR, Linck B, Schmitz W, Scholz H et al. Increased expression of cardiac phosphatases in patients with end-stage heart failure. J Mol Cell Cardiol 1997; 29: 265–272.

2. Bristow MR, Ginsburg R, Minobe W, Cubicciotti R.S, Sageman WS, Lurie K et al. Decreased catecholamine sensitivity and beta-adrenergic-receptor density in failing human hearts. N Engl J Med 1982; 307: 205–211.

3. El-Armouche A, Rau T, Zolk O, Ditz D, Pamminger T, Zimmermann WH et al. Evidence for protein phosphatase inhibitor-1 playing an amplifier role in beta-adrenergic signaling in cardiac myocytes. FASEB J 2003; 17: 437–439.

4. Carr AN, Schmidt AG, Suzuki Y, del Monte F, Sato Y, Lanner C et al. Type 1 phosphatase, a negative regulator of cardiac function. Mol Cell Biol 2002; 22: 4124–4135.

5. Pathak A, del Monte F, Zhao W, Schultz JE, Lorenz JN, Bodi I et al. Enhancement of cardiac function and suppression of heart failure progression by inhibition of protein phosphatase 1. Circ Res 2005; 96: 756–766.

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