Protein kinase D in the hypertrophy pathway
Yuan Yan Sin1, George S Baillie
1Molecular Pharmacology Group, Institute of Cardiovascular and Medical Science, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK. y.sin.1@research.gla.ac.uk
Biochemical Society Transactions
|January 21, 2012
Summary
Protein kinase D (PKD) plays a key role in heart hypertrophy by regulating histone deacetylase 5 (HDAC5) translocation. Understanding this pathway offers potential new treatments for heart failure.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Chronic neurohormonal stimulation adversely affects cardiac structure and function, leading to heart failure.
- Phosphorylation of class II histone deacetylase 5 (HDAC5) is crucial for cardiac gene reprogramming and hypertrophy.
- Protein kinase D (PKD) is implicated in the regulation of HDAC5 translocation.
Purpose of the Study:
- To review recent insights into the role of PKD in cardiac hypertrophic signaling pathways.
- To explore the potential of PKD-mediated mechanisms as therapeutic targets for heart failure.
Main Methods:
- This review summarizes existing experimental findings and recent observations.
- Focuses on the regulatory properties of PKD in HDAC5 phosphorylation and translocation within cardiac cells.
Main Results:
- PKD-mediated regulation of HDAC5 is a significant event in cardiac hypertrophy.
- Recent observations suggest PKD's role in myocardial regulation may offer therapeutic potential.
Conclusions:
- PKD signaling is a critical component of the hypertrophic response in the heart.
- Targeting PKD-mediated pathways presents a promising avenue for developing novel heart failure therapies.
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