| Effect of inhibition of glycogen synthase kinase-3 on cardiac hypertrophy during acute pressure overload. | |
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MedLine Citation:
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PMID: 20549453 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Fumio Yamamoto; Hiroshi Yamamoto |
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Publication Detail:
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Type: Comment; Editorial Date: 2010-06-13 |
Journal Detail:
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Title: General thoracic and cardiovascular surgery Volume: 58 ISSN: 1863-6713 ISO Abbreviation: Gen Thorac Cardiovasc Surg Publication Date: 2010 Jun |
Date Detail:
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Created Date: 2010-06-15 Completed Date: 2010-09-27 Revised Date: 2011-11-02 |
Medline Journal Info:
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Nlm Unique ID: 101303952 Medline TA: Gen Thorac Cardiovasc Surg Country: Japan |
Other Details:
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Languages: eng Pagination: 263-4 Citation Subset: IM |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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:
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Gen Thorac Cardiovasc Surg. 2010 Jun;58(6):265-70
[PMID:
20549454
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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