The aim of the study was to assess urinary transforming growth factor (TGF)-beta1 in children with steroid-dependent nephrotic syndrome (SDNS) treated with cyclosporine A (CyA) and ACE inhibitors (ACEI). The study involved 24 children (14 boys and 10 girls) with SDNS and signs of focal segmental glomerulosclerosis. The children were treated with prednisone, CyA, and ACEI. All children were examined four times: A during relapse of proteinuria, before treatment with CyA and ACEI, and B after 3 months, C 6 months, and D 12 months of treatment. The control group consisted of 20 healthy children of the same age. The urinary TGF-beta1 level was determined by ELISA (R and D Quantikine). The serum CyA level was measured by monoclonal antibody fluorescence polarization immunoassay. Prior to CyA treatment, the urinary TGF-beta1 level was the highest (135.61+/-38.31 pg/mg creatinine). During CyA treatment, TGF-beta1 was reduced to 117.96+/-81.57 after 3 months, to 80.26+/-49.52 after 6 months, and to 44.00+/-31.83 pg/mg creatinine after 12 months, but it was still higher than in the control group. At 3 months there was a positive linear correlation between urinary TGF-beta1 and proteinuria (r=0.654, P<0.01). These results indicate that the urinary TGF-beta1 level increases in proportion to proteinuria during relapse of NS. Treatment with CyA and ACEI also influences urinary TGF-beta1, which is still higher after 12 months of treatment than in healthy children.
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http://dx.doi.org/10.1007/s00467-004-1619-5 | DOI Listing |
PLoS One
January 2025
Department of Kidney Transplantation, Nephropathy Hospital, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaan'xi, China.
Increasing evidence suggests that dysbiosis of gut microbiota exacerbates chronic kidney disease (CKD) progression. Curcumin (CUR) has been reported to alleviate renal fibrosis in animal models of CKD. However, the relationship between CUR and gut microbiome in CKD remains unclear.
View Article and Find Full Text PDFFASEB J
January 2025
Department of Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence, Rhode Island, USA.
Bromodomain-containing protein 4 (BRD4) plays a vital role in fibrosis of various organs. However, the underlying mechanism of BRD4 in renal fibrosis remains unclear. To construct in vitro and in vivo models of renal fibrosis, TCMK-1 cells were subjected to TGF-β1 treatment and mice were subjected to UUO surgery and adenine induction.
View Article and Find Full Text PDFCurr Mol Pharmacol
January 2025
School of Medicine, Yichun University, 576 XueFu Road, Yuanzhou District, Yichun 336000, Jiangxi Province, China.
Background: Finasteride and doxazosin are used for the treatment of benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS). Epithelial-mesenchymal transition (EMT) plays an important role in BPH, little is known about the growth inhibition and anti-fibrosis effects of doxazosin on the regulation of EMT and morphology in the prostate.
Objectives: The present study examined the effects of doxazosin on testosterone propionate (TP)-induced prostate growth in vivo and in vitro and its impact on the EMT and TGF-β/Smad signaling pathway.
Int J Mol Sci
December 2024
MTA-SE Lendület "Momentum" Diabetes Research Group, 1083 Budapest, Hungary.
Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease. Current treatments for DKD do not halt renal injury progression, highlighting an urgent need for therapies targeting key disease mechanisms. Our previous studies demonstrated that activating the Sigma-1 receptor (S1R) with fluvoxamine (FLU) protects against acute kidney injury by inhibiting inflammation and ameliorating the effect of hypoxia.
View Article and Find Full Text PDFMol Med
December 2024
Hebei University of Chinese Medicine, Shijiazhuang, 050091, China.
Nuclear receptor 4A1 (NR4A1) is a gene that increases the likelihood of chronic kidney disease (CKD) and contributes to its development. Previous research has shown that the SAM pointed domain containing Ets transformation-specific transcription factor (SPDEF) can activate NR4A1, but its mechanism of action in renal fibrosis is not yet clear. In this study, we used adenovirus to create a mouse kidney model with a specific knockdown of NR4A1 gene.
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