Hyperhomocysteinemia-induced Dyrk1a downregulation results in cardiomyocyte hypertrophy in rats

Int J Cardiol. 2010 Nov 19;145(2):306-307. doi: 10.1016/j.ijcard.2009.10.043. Epub 2009 Nov 10.

Abstract

Cardiac hypertrophy has been demonstrated in rat models of hyperhomocysteinemia, a major risk factor for chronic heart failure. As one of the molecular pathway which leads to cardiac hypertrophy is mediated by the serine-threonine kinase DYRK1A, we have determined the expression of Dyrk1a in the heart of hyperhomocysteinemic rats and found that hyperhomocysteinemia in rats not only induced ventricular cardiomyocyte hypertrophy but also decreased protein Dyrk1a expression. The decreased expression of Dyrk1a could be consistent with decreased antihypertrophic effects of Dyrk1a leading to cardiomyocyte hypertrophy in case of hyperhomocysteinemia.

Publication types

  • Comparative Study
  • Letter
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cardiomegaly / enzymology*
  • Cardiomegaly / etiology
  • Cardiomegaly / pathology
  • Down-Regulation / physiology*
  • Dyrk Kinases
  • Hyperhomocysteinemia / complications
  • Hyperhomocysteinemia / enzymology*
  • Hyperhomocysteinemia / pathology
  • Myocytes, Cardiac / enzymology*
  • Myocytes, Cardiac / pathology*
  • Protein Serine-Threonine Kinases / antagonists & inhibitors*
  • Protein Serine-Threonine Kinases / biosynthesis
  • Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Protein-Tyrosine Kinases / biosynthesis
  • Rats

Substances

  • Protein-Tyrosine Kinases
  • Protein Serine-Threonine Kinases