Key result
Post-translational modifications of the transcription factor GATA4, such as acetylation and phosphorylation, play a critical role in cardiomyocyte hypertrophy and are promising targets for heart failure therapy.
Targeting the post-translational modifications of the cardiac transcription factor GATA4, such as with p300-specific HAT inhibitors like curcumin, offers a novel therapeutic approach for heart failure.
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GATA4 modulation may offer HF therapy targets; leaves open whether post-translational changes can be exploited clinically.
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.
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Katanasaka et al. (2016) conducted a review in Heart failure and cardiac hypertrophy. GATA4 targeted therapies was evaluated. Post-translational modifications of the transcription factor GATA4, such as acetylation and phosphorylation, play a critical role in cardiomyocyte hypertrophy and are promising targets for heart failure therapy.
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