Soltan Ahmad, Saeed Nazari and Kalantary-Charvadeh, Ashkan and Hamzavi, Masoud and Ezzatifar, Fatemeh and Elmira Aboutalebi Vand Beilankouhi, Elmira Aboutalebi Vand Beilankouhi and Toofani-Milani, Attabak and Geravand, Faezeh and Golshadi, Zakieh and Mesgari-Abbasi, Mehran (2022) TGF-β1 receptor blockade attenuates unilateral ureteral obstruction-induced renal fibrosis in C57BL/6 mice through attenuating Smad and MAPK pathways. Journal of Molecular Histology, 53 (5). pp. 691-698. ISSN 1567-2379
Full text not available from this repository.Abstract
Renal fibrosis is characterized by accumulation of extracellular matrix components and collagen deposition. TGF-β1 acts as a master switch promoting renal fibrosis through Smad dependent and/or Smad independent pathways. Thirty-five male C57BL/6 mice were divided into five groups of seven each; sham, unilateral ureteral obstruction (UUO), UUO+galunisertib (150 and 300 mg/kg/day), galunisertib (300 mg/kg/day). The UUO markedly induced renal fibrosis and injury as indicated by renal functional loss, increased levels of collagen Iα1, fibronectin and α-SMA; it also activated both the Smad 2/3 and MAPKs pathways as indicated by increased levels of TGF-β1, p-Smad 2, p-Smad 3, p-p38, p-JNK and p-ERK. These UUO-induced changes were markedly attenuated by oral administration of galunisertib, the TGFβRI small molecule inhibitor. In conclusion, we demonstrated that TGF-β1 receptor blockade can prevent UUO-induced renal fibrosis through indirect modulation of Smad and MAPKs signaling pathways and may be useful as a therapeutic agent in treatment and/or prevention of renal fibrosis.
| Item Type: | Article |
|---|---|
| Subjects: | QU Biochemistry |
| Divisions: | Faculty of Medicin > Department of Biochemistry |
| Depositing User: | خدیجه شبانکاره |
| Date Deposited: | 10 Oct 2022 10:44 |
| Last Modified: | 10 Oct 2022 10:44 |
| URI: | http://eprints.bpums.ac.ir/id/eprint/9573 |
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