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The protective roles of GLP-1R signaling in diabetic nephropathy: possible mechanism and therapeutic potential.
GLP-1 has a crucial role in protection against increased renal oxidative stress under chronic hyperglycemia, by inhibition of NAD(P)H oxidase, a major source of superoxide, and by cAMP-PKA pathway activation.
Association of monocyte chemoattractant protein-1 with renal tubular damage in diabetic nephropathy.
Reduction of renal superoxide dismutase in progressive diabetic nephropathy.
- H. Fujita, H. Fujishima, Takamune Takahashi
- BiologyJournal of the American Society of Nephrology…
- 1 June 2009
Down-regulation of renal SOD1 and SOD3 may play a key role in the pathogenesis of DN, as observed in the kidneys of diabetic mouse models that exhibit comparable levels of hyperglycemia but different susceptibility to DN.
Stromal cell-derived factor-1 is upregulated by dipeptidyl peptidase-4 inhibition and has protective roles in progressive diabetic nephropathy.
Urinary adiponectin excretion is increased in patients with overt diabetic nephropathy.
Effects of antidiabetic treatment with metformin and insulin on serum and adipose tissue adiponectin levels in db/db mice.
The results suggest that adiponectin synthesis in adipose tissue may be suppressed under hyperinsulinemic state sustained by insulin treatment, even though hyperglycemia is markedly reduced.
SOD1, but not SOD3, deficiency accelerates diabetic renal injury in C57BL/6-Ins2(Akita) diabetic mice.
Modulation of renal superoxide dismutase by telmisartan therapy in C57BL/6-Ins2Akita diabetic mice
It is suggested that NAD(P)H oxidase negatively regulates renal SOD, possibly by downregulation of Nrf2, and that telmisartan could upregulate renal S OD by the suppression of NAD(H) oxidase and subsequent up regulation of NRF2, leading to the amelioration of renal oxidative stress and diabetic renal changes.
Increased Urinary Excretion of Monocyte Chemoattractant Protein-1 in Proteinuric Renal Diseases
It is suggested that heavy proteinuria, itself, probably aggravates renal tubular damage and accelerates the disease progression in diabetic nephropathy by increasing the MCP-1 expression in renal tubuli, irrespective of the types of renal disease.
Effect of metformin on adipose tissue resistin expression in db/db mice.