Activation of general control nonderepressible 2 kinase protects human glomerular endothelial cells from harmful high-glucose-induced molecular pathways

[1]  T. Eleftheriadis,et al.  Differential effects of the two amino acid sensing systems, the GCN2 kinase and the mTOR complex 1, on primary human alloreactive CD4⁺ T-cells. , 2016, International journal of molecular medicine.

[2]  M. Pines,et al.  Halofuginone — The Multifaceted Molecule , 2015, Molecules.

[3]  T. Eleftheriadis,et al.  Indoleamine 2,3-dioxygenase increases p53 levels in alloreactive human T cells, and both indoleamine 2,3-dioxygenase and p53 suppress glucose uptake, glycolysis and proliferation. , 2014, International immunology.

[4]  G. Bray,et al.  FGF21 is an endocrine signal of protein restriction. , 2014, The Journal of clinical investigation.

[5]  Richard C. Silva,et al.  Keeping the eIF2 alpha kinase Gcn2 in check. , 2014, Biochimica et biophysica acta.

[6]  V. D’Agati,et al.  Knockdown of Glyoxalase 1 Mimics Diabetic Nephropathy in Nondiabetic Mice , 2013, Diabetes.

[7]  T. Eleftheriadis,et al.  Inhibition of indoleamine 2,3-dioxygenase in mixed lymphocyte reaction affects glucose influx and enzymes involved in aerobic glycolysis and glutaminolysis in alloreactive T-cells. , 2013, Human immunology.

[8]  C. Sena,et al.  Endothelial dysfunction - a major mediator of diabetic vascular disease. , 2013, Biochimica et biophysica acta.

[9]  T. Eleftheriadis,et al.  The Renal Endothelium in Diabetic Nephropathy , 2013, Renal failure.

[10]  C. Stehouwer,et al.  Glyoxalase-1 overexpression reduces endothelial dysfunction and attenuates early renal impairment in a rat model of diabetes , 2013, Diabetologia.

[11]  M. Cooper,et al.  Mechanisms of diabetic complications. , 2013, Physiological reviews.

[12]  L. Geiss,et al.  Incidence of Treatment for End-Stage Renal Disease Among Individuals With Diabetes in the U.S. Continues to Decline , 2010, Diabetes Care.

[13]  H. Hammes,et al.  Hyperglycemia Impairs Proteasome Function by Methylglyoxal , 2009, Diabetes.

[14]  B. Zinman,et al.  Effect of Protein Kinase Cβ Inhibition on Renal Hemodynamic Function and Urinary Biomarkers in Humans With Type 1 Diabetes: A Pilot Study , 2009, Diabetes Care.

[15]  佐藤 誠也.  Halofuginone prevents extracellular matrix deposition in diabetic nephropathy , 2009 .

[16]  Michael Brownlee,et al.  The pathobiology of diabetic complications: a unifying mechanism. , 2005, Diabetes.

[17]  F. Brosius,et al.  Glucose transporters in diabetic nephropathy , 2005, Pediatric Nephrology.

[18]  L. Rossetti,et al.  Inhibition of GAPDH activity by poly(ADP-ribose) polymerase activates three major pathways of hyperglycemic damage in endothelial cells. , 2003, The Journal of clinical investigation.

[19]  D. Scheuner,et al.  Phosphorylation of the α Subunit of Eukaryotic Initiation Factor 2 Is Required for Activation of NF-κB in Response to Diverse Cellular Stresses , 2003, Molecular and Cellular Biology.

[20]  G. Hart,et al.  O‐GlcNAc turns twenty: functional implications for post‐translational modification of nuclear and cytosolic proteins with a sugar , 2003, FEBS letters.

[21]  D. Scheuner,et al.  Phosphorylation of the alpha subunit of eukaryotic initiation factor 2 is required for activation of NF-kappaB in response to diverse cellular stresses. , 2003, Molecular and cellular biology.

[22]  J. Kirkpatrick.  Albuminuria and Risk of Cardiovascular Events , Death , and Heart Failure in Diabetic and Nondiabetic Individuals , 2002 .

[23]  S. Dimmeler,et al.  Hyperglycemia inhibits endothelial nitric oxide synthase activity by posttranslational modification at the Akt site. , 2001, The Journal of clinical investigation.

[24]  I. G. Fantus,et al.  Hyperglycemia-induced mitochondrial superoxide overproduction activates the hexosamine pathway and induces plasminogen activator inhibitor-1 expression by increasing Sp1 glycosylation. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[25]  Y. Kaneda,et al.  Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage , 2000, Nature.

[26]  G. King,et al.  Amelioration of accelerated diabetic mesangial expansion by treatment with a PKC β inhibitor in diabetic db/db mice, a rodent model for type 2 diabetes , 2000, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[27]  G. King,et al.  Regulation of endothelial constitutive nitric oxide synthase gene expression in endothelial cells and in vivo : a specific vascular action of insulin. , 2000, Circulation.

[28]  U. Sauer,et al.  High glucose-induced transforming growth factor beta1 production is mediated by the hexosamine pathway in porcine glomerular mesangial cells. , 1998, The Journal of clinical investigation.

[29]  G. King,et al.  Characterization of protein kinase C beta isoform activation on the gene expression of transforming growth factor-beta, extracellular matrix components, and prostanoids in the glomeruli of diabetic rats. , 1997, The Journal of clinical investigation.

[30]  P. Tesauro,et al.  Effect of Aldose Reductase Inhibitor (Tolrestat) on Urinary Albumin Excretion Rate and Glomerular Filtration Rate in IDDM Subjects With Nephropathy , 1993, Diabetes Care.

[31]  P. Raskin,et al.  Effect of restricting dietary protein on the progression of renal failure in patients with insulin-dependent diabetes mellitus. , 1991, The New England journal of medicine.

[32]  H. Keen,et al.  RESTRICTION OF DIETARY PROTEIN AND PROGRESSION OF RENAL FAILURE IN DIABETIC NEPHROPATHY , 1989, The Lancet.

[33]  K. Gabbay,et al.  Sorbitol Pathway: Presence in Nerve and Cord with Substrate Accumulation in Diabetes , 1966, Science.