HDL induces NO-dependent vasorelaxation via the lysophospholipid receptor S1P3.
By J. Nofer, M. van der Giet, M. Tölle, Iza Wolinska, Karin von Wnuck Lipinski, H. Baba, U. Tietge, A. Gödecke, I. Ishii, B. Kleuser and 6 more. Journal of Clinical Investigation, 2004
720 citations recorded by the source corpus.
Subfields: Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/3e7549397c4b02bcd448796b743d0cbeac5e5710
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Citations in the corpus
- “Inside-Out” Signaling of Sphingosine-1-Phosphate: Therapeutic Targets (2008, background): “Ample evidence indicates that HDL-bound S1P is biologically active (Nofer et al., 2004; Theilmeier et al., 2006; Matsuo et al., 2007), suggesting that S1P may rapidly associate and dissociate from HDL.”
- Prevalence and characteristics of the metabolic syndrome in women with polycystic ovary syndrome. (2005, neutral): “High BMI (WC) 67 (71) 91 (42) 29 (48) Hypertriglyceridemia 35 (37) 70 (32) 8 (5) Low HDL-C 68 (71) 91 (42) 49 (29) High blood pressure 45 (48) 74 (34) 23 (14) High fasting glucose 3.”
- Endothelium-protective sphingosine-1-phosphate provided by HDL-associated apolipoprotein M (2011, background): “HDLinduced vasorelaxation as well as barrier-promoting and prosurvival actions on the endothelium have been attributed to S1P signaling (2, 4, 13).”
- Functionally Defective High-Density Lipoprotein: A New Therapeutic Target at the Crossroads of Dyslipidemia, Inflammation, and Atherosclerosis (2006, background): “Again, the vasoactive effects of HDL can be mediated by S1P acting via the lysophospholipid receptor S1P3 (Nofer et al., 2004).”