Role of diacylglycerol kinase in cellular regulatory processes: a new regulator for cardiomyocyte hypertrophy

Pharmacol Ther. 2007 Sep;115(3):352-9. doi: 10.1016/j.pharmthera.2007.04.010. Epub 2007 Jun 16.

Abstract

Diacylglycerol (DAG) kinase (DGK) phosphorylates and converts DAG to phosphatidic acid. DGK regulates cellular DAG levels and attenuates DAG signaling. The 10 mammalian DGK isoforms have been identified to date. In cardiac myocytes, DGKalpha, epsilon, and zeta are expressed, and DGKzeta is the predominant isoform. DGKzeta inhibits protein kinase C (PKC) activation and subsequent hypertrophic programs in response to endothelin-1 (ET-1) in neonatal rat cardiomyocytes. DGKzeta blocks cardiac hypertrophy induced by G protein-coupled receptor agonists and pressure overload in vivo. DGKzeta attenuates ventricular remodeling and improves survival after myocardial infarction. These data provide a novel insight for subcellular mechanisms of cardiac hypertrophy and heart failure, and DGKzeta may be a new therapeutic target to prevent cardiac hypertrophy and progression to heart failure.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Diacylglycerol Kinase / genetics
  • Diacylglycerol Kinase / metabolism*
  • Drug Delivery Systems
  • Gene Expression Regulation, Enzymologic*
  • Humans
  • Hypertrophy / genetics
  • Hypertrophy / physiopathology*
  • Isoenzymes
  • Mice
  • Myocardial Infarction / genetics
  • Myocardial Infarction / physiopathology
  • Myocytes, Cardiac / pathology
  • Rats
  • Signal Transduction
  • Ventricular Remodeling / genetics
  • Ventricular Remodeling / physiology

Substances

  • Isoenzymes
  • Diacylglycerol Kinase