cGMP kinase I, cardiac hypertrophy and PDE inhibition

نویسندگان

  • Enrico Patrucco
  • Robert Lukowski
  • Sergei Rybalkin
  • Joe Beavo
  • Franz Hofmann
چکیده

Background The heart responds to maladaptive pro-hypertrophic stimuli by stimulating intrinsic signals that contrast and dampen the onset and development of hypertrophy. Cyclic guanosine monophosphate (cGMP) and its downstream effector cGMP kinase I (cGKI) have been suggested to be an important anti-hypertrophic signalling pathway (1). Intracellular levels of cGMP can be raised by the action of nitric oxide (NO) and natriuretic peptides (ANP, BNP), or by inhibiting cGMP-degrading phosphodiesterases (PDE).

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عنوان ژورنال:

دوره 11  شماره 

صفحات  -

تاریخ انتشار 2011