Document Detail


Effect of inhibition of glycogen synthase kinase-3 on cardiac hypertrophy during acute pressure overload.
MedLine Citation:
PMID:  20549453     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Myocardial hypertrophy has been recognized to be an adaptive response to a variety of external stimuli (e.g., myocardial infarction, pressure overload, catecholamine treatment, endocrine disorders) that are involved in several subcellular factors that mediate signaling pathways, from external stimuli to nuclear protein synthesis. Glycogen synthase kinase-3beta (GSK-3beta) is one of the subcellular factors that regulate nuclear transcription factors, such as activated T-cell (NFAT) proteins, that are related to gene programming during cardiac hypertrophy. On the other hand, GSK-3beta, known as a regulator of cardiomyocyte growth in Wnt signaling of cardiogenesis, is involved in beta-catenin degradation. Inhibition of GSK-3beta has been reported to induce cardiac hypertrophy. Tateishi et al. demonstrated in an aortic constriction-induced acute hypertrophy model using 6-week-old Wister rats that if GSK-3b is inhibited by LiCl up-regulated beta-catenin expression and additional hypertrophy were observed. They suggested that Li(2+) had an additive effect on pressure overload-induced hypertrophy through the GSK-3beta-beta-catenin pathway. Their article provides promising information on the mechanism of hypertrophic myocyte growth during acute pressure overload.
Authors:
Fumio Yamamoto; Hiroshi Yamamoto
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Publication Detail:
Type:  Comment; Editorial     Date:  2010-06-13
Journal Detail:
Title:  General thoracic and cardiovascular surgery     Volume:  58     ISSN:  1863-6713     ISO Abbreviation:  Gen Thorac Cardiovasc Surg     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-06-15     Completed Date:  2010-09-27     Revised Date:  2011-11-02    
Medline Journal Info:
Nlm Unique ID:  101303952     Medline TA:  Gen Thorac Cardiovasc Surg     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  263-4     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Aorta, Abdominal / surgery
Atrial Natriuretic Factor / genetics
Blood Pressure*
Cardiovascular Agents / pharmacology*
Disease Models, Animal
Glycogen Synthase Kinase 3 / antagonists & inhibitors*,  metabolism
Hypertension / complications,  drug therapy*,  enzymology,  physiopathology
Hypertrophy, Left Ventricular / drug therapy*,  enzymology,  etiology,  physiopathology
Ligation
Lithium Chloride / pharmacology*
Phosphorylation
Protein Kinase Inhibitors / pharmacology*
RNA, Messenger / metabolism
Rats
Serine
Time Factors
beta Catenin / metabolism
Chemical
Reg. No./Substance:
0/Cardiovascular Agents; 0/Catnb protein, rat; 0/Protein Kinase Inhibitors; 0/RNA, Messenger; 0/beta Catenin; 56-45-1/Serine; 7447-41-8/Lithium Chloride; 85637-73-6/Atrial Natriuretic Factor; EC 2.7.11.1/glycogen synthase kinase 3 beta; EC 2.7.11.26/Glycogen Synthase Kinase 3
Comments/Corrections
Comment On:
Gen Thorac Cardiovasc Surg. 2010 Jun;58(6):265-70   [PMID:  20549454 ]

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