Signaling pathways for the vascular effects of XXXX .

@entity3958 @entity462 @entity3957 @entity65 @entity855
PURPOSE OF REVIEW: The physiological and pathophysiological importance of endogenous @entity3957 to @entity65 has been recognized in recent years. The signaling mechanisms underlying the multifaceted vascular effects of @entity3958 , on the contrary, have been unclear. This article reviews recent literature on cellular and molecular events triggered or modulated by @entity3958 in the vascular system over the period of 2009-2010. RECENT FINDINGS: @entity3958 causes protein S-sulfhydration. The activation of @entity855 -sensitive K channels (KATP channels) by @entity3958 likely occurs as the result of specific @entity462 residues of KATP channel proteins being S-sulfhydrated. Produced in endothelial cells and inducing smooth muscle hyperpolarization, @entity3958 appears to functioning as an endothelium-derived hyperpolarizing factor. The inhibition of phosphodiesterases by endogenous @entity3958 is an additional exciting discovery, which offers answers for the differential vascular effects of this gasotransmitter due to the tissue-specific distribution of different isozymes of phosphodiesterases. Furthermore, endothelial cells and smooth muscle cells have opposite growth responses to @entity3958 stimulation, involving the same sets of signaling molecules. SUMMARY: An array of signaling pathways in vascular tissues is enlisted by endogenous @entity3958 . An insightful understanding of these signaling mechanisms would help elucidate the pathogenesis of selective @entity65 and develop related therapeutic interventions by targeting @entity3958 metabolism.
