Identificador persistente para citar o vincular este elemento:
http://hdl.handle.net/10662/20226
Títulos: | Targeted disruption of the heat shock protein 20-phosphodiesterase 4D (PDE4D) interaction protects against pathological cardiac remodelling in a mouse model of hypertrophy |
Autores/as: | Martin, Tamara P. Hortigón Vinagre, Maria Pura Findlay, Jane E. Elliot, Christina Currie, Susan Baillie, George |
Palabras clave: | cAMP;PDE4D;HSP20;Cardiac remodeling;Cardiac hypertrophy;Peptide disruption;Remodelación cardiaca;Hipertrofia cardiaca;Alteración de péptidos |
Fecha de publicación: | 2014 |
Editor/a: | Wiley-Blackwell |
Resumen: | Phosphorylated heat shock protein 20 (HSP20) is cardioprotective. Using human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and a mouse model of pressure overload mediated hypertrophy, we show that peptide disruption of the HSP20-phosphodiesterase 4D (PDE4D) complex results in attenuation of action potential prolongation and protection against adverse cardiac remodelling. The later was evidenced by improved contractility, decreased heart weight to body weight ratio, and reduced interstitial and perivascular fibrosis. This study demonstrates that disruption of the specific HSP20-PDE4D interaction leads to attenuation of pathological cardiac remodelling |
URI: | http://hdl.handle.net/10662/20226 |
DOI: | 10.1016/j.fob.2014.10.011 |
Colección: | DBYBM - Artículos |
Archivos
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j_fob_2014_10_011.pdf | 938,13 kB | Adobe PDF | Descargar |
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