The signal pathway for the repressive effect of dipyridamole on myofibroblast transdifferentiation

J Cell Mol Med. 2019 Feb;23(2):1608-1612. doi: 10.1111/jcmm.14006. Epub 2018 Nov 19.
No abstract available

MeSH terms

  • Actins / genetics
  • Actins / metabolism
  • Animals
  • Benzene Derivatives / pharmacology
  • Biomarkers / metabolism
  • Cell Line
  • Cell Transdifferentiation / drug effects*
  • Cell Transdifferentiation / genetics
  • Cyclic AMP / metabolism
  • Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors
  • Cyclic AMP-Dependent Protein Kinases / genetics
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Dipyridamole / pharmacology*
  • Fibroblasts / cytology
  • Fibroblasts / drug effects
  • Fibroblasts / metabolism*
  • Gene Expression Regulation
  • Guanine Nucleotide Exchange Factors / antagonists & inhibitors
  • Guanine Nucleotide Exchange Factors / genetics
  • Guanine Nucleotide Exchange Factors / metabolism
  • Isoquinolines / pharmacology
  • Kidney / cytology
  • Kidney / metabolism
  • Myofibroblasts / cytology
  • Myofibroblasts / drug effects
  • Myofibroblasts / metabolism*
  • Phosphodiesterase Inhibitors / pharmacology*
  • Protein Kinase Inhibitors / pharmacology
  • Rats
  • Signal Transduction*
  • Sulfonamides / pharmacology
  • Sulfones / pharmacology
  • Transforming Growth Factor beta1 / pharmacology

Substances

  • Actins
  • Benzene Derivatives
  • Biomarkers
  • ESI-05
  • Guanine Nucleotide Exchange Factors
  • Isoquinolines
  • Phosphodiesterase Inhibitors
  • Protein Kinase Inhibitors
  • Rapgef3 protein, rat
  • Sulfonamides
  • Sulfones
  • Tgfb1 protein, rat
  • Transforming Growth Factor beta1
  • smooth muscle actin, rat
  • Dipyridamole
  • Cyclic AMP
  • Cyclic AMP-Dependent Protein Kinases
  • N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide