The pathobiology of diabetic complications - A unifying mechanism

[1] Synthesis and secretion of tumour necrosis factor-alpha by human monocytic THP-1 cells and chemotaxis induced by human serum albumin derivatives modified with methylglyoxal and glucose-derived advanced glycation endproducts [J]. IMMUNOLOGY LETTERS, 1997, 58 (03) : 139 - 147

[2] Matrix protein glycation impairs agonist-induced intracellular Ca2+ signaling in endothelial cells [J]. JOURNAL OF CELLULAR PHYSIOLOGY, 2002, 193 (01) : 80 - 92

[3] LAMININ ALTERATIONS AFTER INVITRO NONENZYMATIC GLYCOSYLATION [J]. DIABETES, 1990, 39 (07) : 807 - 814

[4] Diabetes and the accompanying hyperglycemia impairs cardiomyocyte calcium cycling through increased nuclear O-GlcNAcylation [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (45) : 44230 - 44237

[5] ACTIVATION OF PROTEIN-KINASE-C IN GLOMERULAR CELLS IN DIABETES - MECHANISMS AND POTENTIAL LINKS TO THE PATHOGENESIS OF DIABETIC GLOMERULOPATHY [J]. DIABETES, 1994, 43 (01) : 1 - 8

[6] Attenuation of renal injury in db/db mice overexpressing superoxide dismutase -: Evidence for reduced superoxide-nitric oxide interaction [J]. DIABETES, 2004, 53 (03) : 762 - 768

[7] DOI T, 1992, P NATL ACAD SCI USA, V89, P2873, DOI 10.1073/pnas.89.7.2873

[8] Hyperglycemia-induced mitochondrial superoxide overproduction activates the hexosamine pathway and induces plasminogen activator inhibitor-1 expression by increasing Sp1 glycosylation [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (22) : 12222 - 12226

[9] Hyperglycemia inhibits endothelial nitric oxide synthase activity by posttranslational modification at the Akt site [J]. JOURNAL OF CLINICAL INVESTIGATION, 2001, 108 (09) : 1341 - 1348

[10] Du XL, 2003, J CLIN INVEST, V112, P1049, DOI 10.1172/JCI200318127

[1] Synthesis and secretion of tumour necrosis factor-alpha by human monocytic THP-1 cells and chemotaxis induced by human serum albumin derivatives modified with methylglyoxal and glucose-derived advanced glycation endproducts [J]. IMMUNOLOGY LETTERS, 1997, 58 (03) : 139 - 147

[2] Matrix protein glycation impairs agonist-induced intracellular Ca2+ signaling in endothelial cells [J]. JOURNAL OF CELLULAR PHYSIOLOGY, 2002, 193 (01) : 80 - 92

[3] LAMININ ALTERATIONS AFTER INVITRO NONENZYMATIC GLYCOSYLATION [J]. DIABETES, 1990, 39 (07) : 807 - 814

[4] Diabetes and the accompanying hyperglycemia impairs cardiomyocyte calcium cycling through increased nuclear O-GlcNAcylation [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (45) : 44230 - 44237

[5] ACTIVATION OF PROTEIN-KINASE-C IN GLOMERULAR CELLS IN DIABETES - MECHANISMS AND POTENTIAL LINKS TO THE PATHOGENESIS OF DIABETIC GLOMERULOPATHY [J]. DIABETES, 1994, 43 (01) : 1 - 8

[6] Attenuation of renal injury in db/db mice overexpressing superoxide dismutase -: Evidence for reduced superoxide-nitric oxide interaction [J]. DIABETES, 2004, 53 (03) : 762 - 768

[7] DOI T, 1992, P NATL ACAD SCI USA, V89, P2873, DOI 10.1073/pnas.89.7.2873

[8] Hyperglycemia-induced mitochondrial superoxide overproduction activates the hexosamine pathway and induces plasminogen activator inhibitor-1 expression by increasing Sp1 glycosylation [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (22) : 12222 - 12226

[9] Hyperglycemia inhibits endothelial nitric oxide synthase activity by posttranslational modification at the Akt site [J]. JOURNAL OF CLINICAL INVESTIGATION, 2001, 108 (09) : 1341 - 1348

[10] Du XL, 2003, J CLIN INVEST, V112, P1049, DOI 10.1172/JCI200318127