Carlos Félix Sánchez Ferrer-rekin lankidetzan egindako argitalpenak (15)

2017

  1. Erratum to: Inflammation, glucose, and vascular cell damage: The role of the pentose phosphate pathway. [Cardiovasc Diabetol. 15, (2016), (82)] DOI: 10.1186/s12933-016-0397-2

    Cardiovascular Diabetology

2016

  1. Inflammation, glucose, and vascular cell damage: The role of the pentose phosphate pathway

    Cardiovascular Diabetology, Vol. 15, Núm. 1

2014

  1. Abstract 560: Inflammation Converts Glucose Into A Deleterious Agent In Human Aortic Smooth Muscle Cells

    Hypertension, Vol. 64, Núm. suppl_1

2013

  1. Complete blockade of the vasorelaxant effects of angiotensin-(1-7) and bradykinin in murine microvessels by antagonists of the receptor Mas

    Journal of Physiology, Vol. 591, Núm. 9, pp. 2275-2285

2011

  1. Pathways responsible for apoptosis resulting from Amadori-induced oxidative and nitrosative stress in human mesothelial cells

    American Journal of Nephrology, Vol. 34, Núm. 2, pp. 104-114

2010

  1. Inflammation determines the pro-adhesive properties of high extracellular D-glucose in human endothelial cells in vitro and rat microvessels in vivo

    PLoS ONE, Vol. 5, Núm. 4

2009

  1. Extracellular PBEF/NAMPT/visfatin activates pro-inflammatory signalling in human vascular smooth muscle cells through nicotinamide phosphoribosyltransferase activity

    Diabetologia, Vol. 52, Núm. 11, pp. 2455-2463

2008

  1. The deleterious effect of high concentrations of D-glucose requires pro-inflammatory preconditioning

    Journal of Hypertension, Vol. 26, Núm. 3, pp. 478-485

2007

  1. Endothelial dysfunction through genetic deletion or inhibition of the G protein-coupled receptor Mas: A new target to improve endothelial function

    Journal of Hypertension, Vol. 25, Núm. 12, pp. 2421-2425

  2. Xanthine oxidase-derived extracellular superoxide anions stimulate activator protein 1 activity and hypertrophy in human vascular smooth muscle via c-Jun N-terminal kinase and p38 mitogen-activated protein kinases

    Journal of Hypertension, Vol. 25, Núm. 3, pp. 609-618

2006

  1. 345 Endothelial dysfunction by genetic deletion or inhibition of the G prteoin-coupled receptor Mas — a new target to improve endothelial function

    European Journal of Heart Failure Supplements, Vol. 5, Núm. 1, pp. 73

  2. Pro-inflammatory effects of early non-enzymatic glycated proteins in human mesothelial cells vary with cell donor's age

    British Journal of Pharmacology, Vol. 149, Núm. 8, pp. 979-987

2005

  1. Amadori adducts activate nuclear factor-κB-related proinflammatory genes in cultured human peritoneal mesothelial cells

    British Journal of Pharmacology, Vol. 146, Núm. 2, pp. 268-279

  2. Evidence for sodium azide as an artifact mediating the modulation of inducible nitric oxide synthase by C-reactive protein

    Journal of Cardiovascular Pharmacology, Vol. 45, Núm. 3, pp. 193-196

2003

  1. Glycosylated human oxyhaemoglobin activates nuclear factor-κB and activator protein-1 in cultured human aortic smooth muscle

    British Journal of Pharmacology, Vol. 140, Núm. 4, pp. 681-690