Cardiac-specific overexpression of E40K active Akt prevents pressure overload-induced heart failure in mice by increasing angiogenesis and reducing apoptosis

Ceci, M; Gallo, P; Santonastasi, M; Grimaldi, S; Latronico, M V G; Pitisci, A; Missol-Kolka, E; Scimia, M C; Catalucci, D; Hilfiker-Kleiner, D; Condorelli, G

doi:10.1038/sj.cdd.4402095

Letter to the Editor
Published: 19 January 2007

Cardiac-specific overexpression of E40K active Akt prevents pressure overload-induced heart failure in mice by increasing angiogenesis and reducing apoptosis

M Ceci¹^na1,
P Gallo^2,3^na1,
M Santonastasi^1,3^na1,
S Grimaldi^1,3,
M V G Latronico¹,
A Pitisci^1,3,
E Missol-Kolka⁴,
M C Scimia^1,5,
D Catalucci^1,5,
D Hilfiker-Kleiner⁴ &
…
G Condorelli^1,5

Cell Death & Differentiation volume 14, pages 1060–1062 (2007)Cite this article

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Dear Editor,

Physiological myocardial hypertrophy is the result of adaptation of the heart to increased work demands on the cardiovascular system. This response is mediated by pathways which trigger increased protein synthesis and the consequent growth in cardiomyocyte (CMC) size. Multiple signaling pathways contribute to the physiological hypertrophy phenotype, of which one well studied is the IGF1-PI3K-Akt pathway.¹ This pathway is also involved in the mechanism of action of pro-angiogenic factors like vascular endothelial growth factor (VEGF), and leads to capillary formation and migration.^{1, 2}

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Acknowledgements

GC is supported by grants from the NIH (RO HL078797-01A1), the European Community (EU FP6 grant LSHM-CT-2005-018833, EUGeneHeart), Italian Ministry of Health, Italian Ministry of Research and University. DC is supported by a Marie Curie International Fellowship within the 6th European Framework Programme.

Author information

M Ceci, P Gallo and M Santonastasi: These authors contributed equally to this work

Authors and Affiliations

I.R.C.C.S. Multimedica, Milan, Italy
M Ceci, M Santonastasi, S Grimaldi, M V G Latronico, A Pitisci, M C Scimia, D Catalucci & G Condorelli
University Campus Biomedico, Rome, Italy
P Gallo
San Raffaele Biomedical Science Park Foundation, Rome, Italy
P Gallo, M Santonastasi, S Grimaldi & A Pitisci
Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
E Missol-Kolka & D Hilfiker-Kleiner
Department of Medicine, Division of Cardiology, University of California San Diego, La Jolla, USA
M C Scimia, D Catalucci & G Condorelli

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M Ceci
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P Gallo
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M Santonastasi
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S Grimaldi
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M V G Latronico
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A Pitisci
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E Missol-Kolka
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M C Scimia
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D Catalucci
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D Hilfiker-Kleiner
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G Condorelli
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Corresponding author

Correspondence to G Condorelli.

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Supplementary Information accompanies the paper on Cell Death and Differentiation website (http://www.nature.com/cdd)

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Ceci, M., Gallo, P., Santonastasi, M. et al. Cardiac-specific overexpression of E40K active Akt prevents pressure overload-induced heart failure in mice by increasing angiogenesis and reducing apoptosis. Cell Death Differ 14, 1060–1062 (2007). https://doi.org/10.1038/sj.cdd.4402095

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Published: 19 January 2007
Issue date: 01 May 2007
DOI: https://doi.org/10.1038/sj.cdd.4402095

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Cardiac-specific overexpression of E40K active Akt prevents pressure overload-induced heart failure in mice by increasing angiogenesis and reducing apoptosis

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Supplementary Information (DOC 2203 kb)

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Danlou Tablet Protects Against Cardiac Remodeling and Dysfunction after Myocardial Ischemia/Reperfusion Injury through Activating AKT/FoxO3a Pathway

The antioxidant compound tert-butylhydroquinone activates Akt in myocardium, suppresses apoptosis and ameliorates pressure overload-induced cardiac dysfunction

Increased cardiac remodeling in cardiac-specific Flt-1 receptor knockout mice with pressure overload

Akt mediated mitochondrial protection in the heart: metabolic and survival pathways to the rescue

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References

Acknowledgements

Author information

Authors and Affiliations

Corresponding author

Additional information

Supplementary information

Supplementary Information (DOC 2203 kb)

Rights and permissions

About this article

Cite this article

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This article is cited by

Danlou Tablet Protects Against Cardiac Remodeling and Dysfunction after Myocardial Ischemia/Reperfusion Injury through Activating AKT/FoxO3a Pathway

The antioxidant compound tert-butylhydroquinone activates Akt in myocardium, suppresses apoptosis and ameliorates pressure overload-induced cardiac dysfunction

Increased cardiac remodeling in cardiac-specific Flt-1 receptor knockout mice with pressure overload

Akt mediated mitochondrial protection in the heart: metabolic and survival pathways to the rescue

Search

Quick links