<b>Results:</b> DDR2 expression was dramatically increased in the obstructed kidney; In contrast to wild-type mice that developed severe interstitial fibrosis, the DDR2-deficient mice displayed only moderate fibrotic changes; Compared with the UUO group, the degree of renal interstitial fibrosis in CDT group was relieved after operation 14 day.
<i>In vivo</i>, administration of BT173 decreased Smad3 phosphorylation and mitigated renal fibrosis and deposition of extracellular matrix in unilateral ureteral obstruction and Tg26 mouse models of renal fibrosis.
15d-PGJ<sub>2</sub> increased NF-E2-related nuclear factor erythroid-2 (Nrf2) protein expression in response to UUO, and heme oxygenase 1 (HO-1), a downstream target of Nrf2, was induced by 15d-PGJ<sub>2</sub>.
15d-PGJ<sub>2</sub> increased NF-E2-related nuclear factor erythroid-2 (Nrf2) protein expression in response to UUO, and heme oxygenase 1 (HO-1), a downstream target of Nrf2, was induced by 15d-PGJ<sub>2</sub>.
Jagged-1 expression was significantly increased in the kidneys of normal mice treated with TGF-beta1 and was decreased in the kidneys of mice with UUO treated with a TGF-beta receptor II-Fc chimera.
GADD45gamma was strongly expressed in as little as 6 h following ureteric obstruction in the renal tubules, and was also found in kidney tissue of patients with chronic glomerulonephritis.
TSP-1 shRNA suppressed the protein level of TSP-1, increased VEGF expression and PTC density and alleviated the development of renal interstitial fibrosis in UUO mice.
TSP-1 shRNA suppressed the protein level of TSP-1, increased VEGF expression and PTC density and alleviated the development of renal interstitial fibrosis in UUO mice.
TSP-1 shRNA suppressed the protein level of TSP-1, increased VEGF expression and PTC density and alleviated the development of renal interstitial fibrosis in UUO mice.
TSP-1 shRNA suppressed the protein level of TSP-1, increased VEGF expression and PTC density and alleviated the development of renal interstitial fibrosis in UUO mice.
RGC-32 knockdown by shRNA significantly inhibits UUO-induced renal structural damage, α-SMA expression and collagen deposition, suggesting that RGC-32 is essential for the onset of renal interstitial fibrosis.
AMPKα2 deficiency also increased the expression of chemokines KC and MCP-1, along with enhanced infiltration of inflammatory cells into the kidney after UUO.
Gal-3 has been studied in experimental acute kidney damage and in the subsequent regeneration phase as well as in several models of chronic kidney disease, including nephropathies induced by aging, ischemia, hypertension, diabetes, hyperlipidemia, unilateral ureteral obstruction and chronic allograft injury.