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HMGCR — NOS3

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: NOS3 → HMGCR (decreases, HMGCR Activity, NOS3 Activity)
  Evidence: Previous studies indicate that 3-hydroxy-3-methylglutaryl-coenzyme A (HMG CoA) reductase inhibitors improve endothelium-dependent relaxation by increasing ecNOS activity.

Text-mined interactions from Literome

Sata et al., FASEB J 2001 (Ischemia) : Endothelial nitric oxide synthase is essential for the HMG-CoA reductase inhibitor cerivastatin to promote collateral growth in response to ischemia
Yamamoto et al., Atherosclerosis 2003 : HMG-CoA reductase inhibitor enhances inducible nitric oxide synthase expression in rat vascular smooth muscle cells ; involvement of the Rho/Rho kinase pathway
Huang et al., J Biomed Sci 2003 : HMG-CoA reductase inhibitors inhibit inducible nitric oxide synthase gene expression in macrophages
Varela et al., J Am Soc Nephrol 2004 : Statins, 3-hydroxy-3-methylglutaryl CoA reductase inhibitors, acutely increase endothelial nitric oxide synthase (eNOS) activity and chronically increase eNOS expression in endothelial cells
Suh et al., J Korean Med Sci 2010 (Hypertension) : Furthermore, HMG-CoA reductase inhibitor can activate the eNOS by phosphorylation related to decreased caveolin-1 abundance
Laufs et al., Circulation 1998 (Arteriosclerosis) : Upregulation of endothelial nitric oxide synthase by HMG CoA reductase inhibitors ... Inhibition of endothelial HMG CoA reductase upregulates ecNOS expression predominantly by posttranscriptional mechanisms
Endres et al., Proc Natl Acad Sci U S A 1998 (Ischemic Attack, Transient) : The up-regulation of eNOS by HMG-CoA reductase inhibitors is not associated with changes in serum cholesterol levels, but is reversed by cotreatment with L-mevalonate and by the downstream isoprenoid, geranylgeranyl pyrophosphate and not by farnesyl pyrophosphate