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Gogiraju, Rajinikanth [Author] ; Dobbelstein, Matthias [Degree supervisor]; Kessel, Michael [Degree supervisor]; Zimmermann, Wolfram-Hubertus [Degree supervisor]; Zeisberg, Michael [Degree supervisor]; Lutz, Susanne [Degree supervisor]; Schäfer, Katrin [Degree supervisor]

Endothelial transformation related protein 53 deletion promotes angiogenesis and prevents cardiac fibrosis and heart failure induced by pressure overload in mice

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  • Media type: E-Book; Thesis
  • Title: Endothelial transformation related protein 53 deletion promotes angiogenesis and prevents cardiac fibrosis and heart failure induced by pressure overload in mice
  • Contributor: Gogiraju, Rajinikanth [Author]; Dobbelstein, Matthias [Degree supervisor]; Kessel, Michael [Degree supervisor]; Zimmermann, Wolfram-Hubertus [Degree supervisor]; Zeisberg, Michael [Degree supervisor]; Lutz, Susanne [Degree supervisor]; Schäfer, Katrin [Degree supervisor]
  • Published: 2015
  • Extent: Online-Ressource
  • Language: English
  • Identifier:
  • Keywords: Hochschulschrift
  • Origination:
  • University thesis: Dissertation, Georg-August-Universität Göttingen, 2015
  • Footnote:
  • Description: Background− Accumulation of transformation related protein 53 (p53), apoptotic cell death and rarefication of myocardial angiogenesis may be involved in the development of cardiac dysfunction during chronic pressure overload. Objective− The aim of this study was to determine whether prevention of endothelial cell apoptosis deletion of p53 in endothelial cells improves cardiac remodeling during pressure overload and prevents the transition from hypertrophy to heart failure. Methods and Results− Mice with endothelial deletion of p53 (End.p53-KO) were generated by crossing p53fl/fl mice with ...
  • Access State: Open Access