D-ribose induces nephropathy through RAGE-dependent NF-jB inflammation
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D-ribose induces nephropathy through RAGE-dependent NF-jB inflammation' 의 참고문헌
Tubular NF-kappa B and AP-1 activation in human proteinuric renal disease
The proximal tubule in the pathophysiology of the diabetic kidney
The axis AGE-RAGE-soluble RAGE and oxidative stress in chronic kidney disease;Oxidative stress and inflammation in non-communicable diseases-molecular mechanisms and perspectives in therapeutics, vol 824
The AGE-receptor in the pathogenesis of diabetic complications
Stimulation of insulin secretion in the rabbit by D-ribose
Role of inflammation in diabetic complications
Role of NF-kappa B in the pathogenesis of diabetes and its associated complications
Ribosylation rapidly induces alpha-synuclein to form highly cytotoxic molten globules of advanced glycation end products
Receptor for advanced glycation endproducts (RAGE) exhibits highly differential cellular and subcellular localisation in rat and human lung
Receptor for AGEs (RAGE) blockade may exert its renoprotective effects in patients with diabetic nephropathy via induction of the angiotensin II type 2 (AT2) receptor
Rapid glycation with D-ribose induces globular amyloid-like aggregations of BSA with high cytotoxicity to SH-SY5Y cells
RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathy
Profound mishandling of protein glycation degradation products in uremia and dialysis
Oral administration of D-ribose in diabetes mellitus
NF-kappaB: linking inflammation and immunity to cancer development and progression
NF-kappa B activation and overexpression of regulated genes in human diabetic nephropathy
Long-term dietary antioxidant cocktail supplementation effectively reduces renal inflammation in diabetic mice
Long-term administration of advanced glycation end-product stimulates the activation of NLRP3 inflammasome and sparking the development of renal injury
Jiangtang decoction ameliorate diabetic nephropathy through the regulation of PI3K/Akt-mediated NF-kappa B pathways in KK-Ay mice
Inhibition of nuclear factor-kappa B activation by pyrrolidine dithiocarbamate prevents chronic FK506 nephropathy
Immune and inflammatory role in renal disease
IL-6 receptor blockade ameliorates diabetic nephropathy via inhibiting inflammasome in mice
IKK-1 and IKK-2: cytokine-activated I kappa B kinases essential for NF-kappa B activation
Hypoglycemic effect of D-ribose in man
Gavage of D-ribose induces Ab-like deposits, Tau hyperphosphorylation as well as memory loss and anxiety-like behavior in mice
GRP75 of CHO cells responds to ribosylation
Expression of advanced glycation end products and their cellular receptor RAGE in diabetic nephropathy and nondiabetic renal disease
Enhanced expression of receptor for advanced glycation end products in chronic kidney disease
Enalapril reduces the expression of nuclear factor-kappa B and c-Jun N-terminal kinase in the renal cortices of five-sixths-nephrectomized rats
D-ribosylation induces cognitive impairment through RAGE-dependent astrocytic inflammation
D-ribosylated Tau forms globular aggregates with high cytotoxicity
D-ribose induces cellular protein glycation and impairs mouse spatial cognition
D-ribose in glycation and protein aggregation
D-Ribose glycates beta(2)-microglobulin to form aggregates with high cytotoxicity through a ROS-mediated pathway
BAY 11-7082 ameliorates diabetic nephropathy by attenuating hyperglycemia-mediated oxidative stress and renal inflammation via NF-kappa B pathway
AGEs, rather than hyperglycemia, are responsible for microvascular complications in diabetes: a "glycoxidation-centric" point of view
A cytokine-responsive I kappa B kinase that activates the transcription factor NF-kappa B
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D-ribose induces nephropathy through RAGE-dependent NF-jB inflammation'
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