S-Nitrosothiols—NO donors regulating cardiovascular cell proliferation: Insight into intracellular pathway alterations

• cGMP dependent and independent mechanism of NO based signaling pathways modulates vascular cell proliferation
• cGMP independent mechanism occurs through cysteine S-nitrosation and S-glutathionylation, tyrosine nitration of proteins.
• Further insight into NO based signaling pathway can be found at http://www.sfrbm.org/sections/education/frs-presentations.

Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) activates signaling pathways responsible for smooth muscle cell relaxation, leading to vasodilation and thus plays an important role in controlling vascular homeostasis, thrombosis and inflammation.Recent studies indicate that S-nitrosothiols produced in vivo as well as synthetic ones might be important reservoirs of NO. Based on a broad range of NO functions within the living organisms, this review highlights the impact of S-nitrosothiols on cardiovascular cell cycle. The cell membrane transport and the decomposition patterns responsible of S-nitrosothiols actions are presented. The effects of NO delivery through S-nitrosothiols have a significant potential in cardiovascular diseases with various underlying causes. The challenges related to their application in the pharmacotherapy of patients with various cardiovascular diseases are also discussed.