Regulation of Cardiac Transcription Factor GATA4 by Post-Translational Modification in Cardiomyocyte Hypertrophy and Heart Failure.
Heart failure is a leading cause of cardiovascular mortality in industrialized countries. During development and deterioration of heart failure, cardiomyocytes undergo maladaptive hypertrophy, and changes in the cellular phenotype are accompanied by reinduction of the fetal gene program. Gene expression in cardiomyocytes is regulated by various nuclear transcription factors, co-activators, and co-repressors. The zinc finger protein GATA4 is one such transcription factor involved in the regulation of cardiomyocyte hypertrophy. In response to hypertrophic stimuli such as those involving the sympathetic nervous and renin-angiotensin systems, changes in protein interaction and/or post-translational modifications of GATA4 cause hypertrophic gene transcription in cardiomyocytes. In this article, we focus on cardiac nuclear signaling molecules, especially GATA4, that are promising as potential targets for heart failure therapy.
Division of Molecular Medicine, School of Pharmaceutical Sciences, University of Shizuoka.
Yasufumi
Y
Katanasaka
Hidetoshi
H
Suzuki
Yoichi
Y
Sunagawa
Koji
K
Hasegawa
Tatsuya
T
Morimoto
D006332:Cardiomegaly / Q000209:etiology*; D050991:GATA4 Transcription Factor / Q000378:metabolism*; D006333:Heart Failure / Q000209:etiology*; D006801:Humans; D032383:Myocytes, Cardiac / Q000473:pathology*; D011499:Protein Processing, Post-Translational
D050991:GATA4 Transcription Factor