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ENPP1 Q121 Variant, Increased Pulse Pressure and Reduced Insulin Signaling, and Nitric Oxide Synthase Activity in Endothelial Cells
Author(s) -
Simonetta Bacci,
Rosa Di Paola,
Claudia Menzaghi,
Patrizia Di Fulvio,
Sara Di Silvestre,
Fabio Pellegrini,
Roberto Baratta,
Antonella Marucci,
Sandra Mastroianno,
G. Fini,
Gloria Formoso,
Agostino Consoli,
Francesco Perticone,
Lucia Frittitta,
Assunta Pandolfi,
Vincenzo Trischitta
Publication year - 2009
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.109.189191
Subject(s) - insulin resistance , endocrinology , medicine , insulin , autophosphorylation , insulin receptor , nitric oxide , protein kinase b , endothelial dysfunction , heritability , nitric oxide synthase , biology , phosphorylation , biochemistry , genetics , protein kinase a
Insulin resistance induces increased pulse pressure (PP), endothelial dysfunction (ED), and reduced bioavailability of endothelium-derived nitric oxide (NO). The genetic background of these 3 cardiovascular risk factors might be partly common. The ENPP1 K121Q polymorphism is associated with insulin resistance and cardiovascular risk.

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