Document Detail


Myocardial AKT: the omnipresent nexus.
MedLine Citation:
PMID:  21742795     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
One of the greatest examples of integrated signal transduction is revealed by examination of effects mediated by AKT kinase in myocardial biology. Positioned at the intersection of multiple afferent and efferent signals, AKT exemplifies a molecular sensing node that coordinates dynamic responses of the cell in literally every aspect of biological responses. The balanced and nuanced nature of homeostatic signaling is particularly essential within the myocardial context, where regulation of survival, energy production, contractility, and response to pathological stress all flow through the nexus of AKT activation or repression. Equally important, the loss of regulated AKT activity is primarily the cause or consequence of pathological conditions leading to remodeling of the heart and eventual decompensation. This review presents an overview compendium of the complex world of myocardial AKT biology gleaned from more than a decade of research. Summarization of the widespread influence that AKT exerts upon myocardial responses leaves no doubt that the participation of AKT in molecular signaling will need to be reckoned with as a seemingly omnipresent regulator of myocardial molecular biological responses.
Authors:
Mark A Sussman; Mirko Völkers; Kimberlee Fischer; Brandi Bailey; Christopher T Cottage; Shabana Din; Natalie Gude; Daniele Avitabile; Roberto Alvarez; Balaji Sundararaman; Pearl Quijada; Matt Mason; Mathias H Konstandin; Amy Malhowski; Zhaokang Cheng; Mohsin Khan; Michael McGregor
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Physiological reviews     Volume:  91     ISSN:  1522-1210     ISO Abbreviation:  Physiol. Rev.     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-07-11     Completed Date:  2011-09-06     Revised Date:  2013-06-28    
Medline Journal Info:
Nlm Unique ID:  0231714     Medline TA:  Physiol Rev     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1023-70     Citation Subset:  IM    
Affiliation:
Department of Biology, San Diego State University, SDSU Heart Institute, San Diego, California 92182, USA. sussman@heart.sdsu.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Calcium Signaling / physiology
Cardiomyopathies / physiopathology
Cell Survival / physiology
Enzyme Activation
Humans
MicroRNAs / metabolism
Mitochondria / enzymology
Myocardial Contraction / physiology
Myocardium / enzymology*
Neovascularization, Physiologic / physiology
Protein Kinases / metabolism
Proto-Oncogene Proteins c-akt / metabolism*
Proto-Oncogene Proteins c-pim-1 / metabolism
Sex Characteristics
Signal Transduction / physiology
Grant Support
ID/Acronym/Agency:
1 R21 HL104544-01/HL/NHLBI NIH HHS; 1R21HL102714-01/HL/NHLBI NIH HHS; 2 R01HL067245/HL/NHLBI NIH HHS; IR37 HL091102-01/HL/NHLBI NIH HHS; P01 HL085577/HL/NHLBI NIH HHS; P01HL085577-05/HL/NHLBI NIH HHS; R01 HL067245/HL/NHLBI NIH HHS; R01 HL105759/HL/NHLBI NIH HHS; R21 HL102613/HL/NHLBI NIH HHS; R21 HL102613-01/HL/NHLBI NIH HHS; R21 HL102714/HL/NHLBI NIH HHS; R21 HL104544/HL/NHLBI NIH HHS; R37 HL091102/HL/NHLBI NIH HHS; RC1 HL100891/HL/NHLBI NIH HHS; RC1HL100891-02/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/MicroRNAs; EC 2.7.-/Protein Kinases; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.1/Proto-Oncogene Proteins c-pim-1
Comments/Corrections

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