Document Detail


Upregulation of heat shock transcription factor 1 plays a critical role in adaptive cardiac hypertrophy.
MedLine Citation:
PMID:  17095722     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Exercise-induced cardiac hypertrophy has been reported to have better prognosis than pressure overload-induced cardiac hypertrophy. Cardiac hypertrophy induced by exercise was associated with less cardiac fibrosis and better systolic function, suggesting that the adaptive mechanisms may exist in exercise-induced hypertrophy. Here, we showed a critical role of heat shock transcription factor 1 (HSF1), an important transcription factor for heat shock proteins, in the adaptive mechanism of cardiac hypertrophy. We examined expression of 8800 genes in the heart of exercise-induced hypertrophy model using DNA chip technique and compared with pressure overload-induced hypertrophy. Expression of HSF1 and its target molecule heat shock proteins was significantly upregulated in the heart by exercise but not by chronic pressure overload. Constitutive activation of HSF1 in the heart significantly ameliorated death of cardiomyocytes and cardiac fibrosis and thereby prevented cardiac dysfunction as well as hypertrophy induced by chronic pressure overload. Conversely, decreased activity of HSF1 in the heart promoted cardiac dysfunction in response to exercise, a load that normally leads to adaptive hypertrophy with preserved systolic function. Likewise, cardiac function was significantly impaired from the early phase of pressure overload, when HSF1 activation was inhibited. These results suggest that HSF1 plays a critical role in the transition between adaptive and maladaptive hypertrophy.
Authors:
Masaya Sakamoto; Tohru Minamino; Haruhiro Toko; Yosuke Kayama; Yunzeng Zou; Masanori Sano; Eiichi Takaki; Teruhiko Aoyagi; Katsuyoshi Tojo; Naoko Tajima; Akira Nakai; Hiroyuki Aburatani; Issei Komuro
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-11-09
Journal Detail:
Title:  Circulation research     Volume:  99     ISSN:  1524-4571     ISO Abbreviation:  Circ. Res.     Publication Date:  2006 Dec 
Date Detail:
Created Date:  2006-12-12     Completed Date:  2007-01-05     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1411-8     Citation Subset:  IM    
Affiliation:
Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological / physiology*
Animals
Aorta, Abdominal
Blood Pressure
Cardiomegaly / pathology,  physiopathology*
DNA-Binding Proteins / genetics*,  metabolism
Disease Models, Animal
Fibrosis
Gene Expression
HSP72 Heat-Shock Proteins / genetics,  metabolism
Heart Failure / pathology,  physiopathology*
Ligation
Male
Myocardium / pathology
Oligonucleotide Array Sequence Analysis
Organ Size
Physical Exertion
Rats
Rats, Wistar
Transcription Factors / genetics*,  metabolism
Up-Regulation
Chemical
Reg. No./Substance:
0/DNA-Binding Proteins; 0/HSP72 Heat-Shock Proteins; 0/Transcription Factors; 0/heat shock transcription factor
Comments/Corrections
Comment In:
Circ Res. 2007 Feb 16;100(3):e45-6   [PMID:  17307965 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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