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An increasingly used animal model of obstructive nephropathy is unilateral ureteral obstruction (UUO).
Ureteropelvic junction obstruction is a common cause of congenital obstructive nephropathy.
Obstructive nephropathy: Insights from genetically engineered animals.
Multifunctionality of PAI-1 in fibrogenesis: Evidence from obstructive nephropathy in PAI-1 overexpressing PAI-1 overexpressing
Congenital obstructive nephropathy is the primary cause for end-stage renal disease (ESRD) in children.
During the last decade genetically modified animals are increasingly used to study the development of obstructive nephropathy.
Further use of these animals, especially in combination with pharmacologic tools, should help to better identify potential antifibrotic strategies in obstructive nephropathy.
The clinical tests currently in use for obstructive nephropathy (such as renal ultrasonography, differential radionuclide renal scans and urinary creatinine concentration data) are not efficient predictors of the subsequent clinical course.
This model mimics, in an accelerated manner, the different stages of obstructive nephropathy leading to tubulointerstitial fibrosis: cellular infiltration, tubular proliferation and apoptosis, epithelial-mesenchymal transition (EMT), (myo)fibroblast accumulation, increased extracellular matrix (ECM) deposition, and tubular atrophy.
In addition, we investigated the role of TLR2 in inflammation during obstructive nephropathy.
To further explore the role of TLR2 during obstructive nephropathy, we additionally analyzed the amount of myofibroblasts (α-SMA).
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