Document Detail


Many good reasons to have STAT3 in the heart.
MedLine Citation:
PMID:  15963355     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The transcription factor signal transducer and activator of transcription 3 (STAT3) participates in a wide variety of physiological processes and directs seemingly contradictory responses, such as proliferation and apoptosis. The constitutive activation of STAT3 promotes tumor growth and angiogenesis and is associated with drug resistance in cancer therapy. In contrast, in the heart, the down-regulation of STAT3 has been associated with end-stage heart failure in patients. Moreover, multiple studies showed that the activation of STAT3 promotes cardiomyocyte survival and hypertrophy, as well as cardiac angiogenesis, in response to various pathophysiologic stimuli, strongly suggesting that STAT3 is beneficial for the heart. Conditional knockout (STAT3-KO) mice harboring a cardiomyocyte-restricted deletion of STAT3 showed enhanced susceptibility to cardiac injury caused by myocardial ischemia, systemic inflammation, or drug toxicity. STAT3-KO mice were also more prone to the pathogenesis of age-related heart failure. Thus, STAT3 is involved in multiple mechanisms required for the protection of the heart from injury and heart failure. These observations should be taken into account in designing novel therapeutic strategies for the prevention of cardiac failure.
Authors:
Denise Hilfiker-Kleiner; Andres Hilfiker; Helmut Drexler
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2005-04-21
Journal Detail:
Title:  Pharmacology & therapeutics     Volume:  107     ISSN:  0163-7258     ISO Abbreviation:  Pharmacol. Ther.     Publication Date:  2005 Jul 
Date Detail:
Created Date:  2005-06-20     Completed Date:  2005-10-05     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  7905840     Medline TA:  Pharmacol Ther     Country:  England    
Other Details:
Languages:  eng     Pagination:  131-7     Citation Subset:  IM    
Affiliation:
Department of Cardiology and Angiology, Medical School Hannover, Carl-Neuberg Str. 1, Hannover 30625, Germany. hilfiker.denise@mh-hannover.de
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MeSH Terms
Descriptor/Qualifier:
Animals
DNA-Binding Proteins / pharmacology,  physiology*,  therapeutic use
Heart Failure* / etiology,  physiopathology,  prevention & control
Humans
Neoplasms / drug therapy
STAT3 Transcription Factor
Signal Transduction / drug effects*,  physiology
Trans-Activators / pharmacology,  physiology*,  therapeutic use
Chemical
Reg. No./Substance:
0/DNA-Binding Proteins; 0/STAT3 Transcription Factor; 0/STAT3 protein, human; 0/Trans-Activators

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


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