Title : A Rho kinase inhibitor (Fasudil) suppresses TGF-β mediated autophagy in urethra fibroblasts to attenuate traumatic urethral stricture (TUS) through re-activating Akt/mTOR pathway: An in vitro study.

Pub. Date : 2021 Feb 15

PMID : 33373654






6 Functional Relationships(s)
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1 A Rho kinase inhibitor (Fasudil) suppresses TGF-beta mediated autophagy in urethra fibroblasts to attenuate traumatic urethral stricture (TUS) through re-activating Akt/mTOR pathway: An in vitro study. fasudil AKT serine/threonine kinase 1 Homo sapiens
2 In addition, TGF-beta treatment decreased the expression levels of phosphorylated Akt (p-Akt) and mTOR (p-mTOR) to inactivate the Akt/mTOR pathway in the PUFs, which could be re-activated by Fasudil. fasudil AKT serine/threonine kinase 1 Homo sapiens
3 In addition, TGF-beta treatment decreased the expression levels of phosphorylated Akt (p-Akt) and mTOR (p-mTOR) to inactivate the Akt/mTOR pathway in the PUFs, which could be re-activated by Fasudil. fasudil AKT serine/threonine kinase 1 Homo sapiens
4 In addition, TGF-beta treatment decreased the expression levels of phosphorylated Akt (p-Akt) and mTOR (p-mTOR) to inactivate the Akt/mTOR pathway in the PUFs, which could be re-activated by Fasudil. fasudil AKT serine/threonine kinase 1 Homo sapiens
5 Then, the fibroblasts were treated with the Pan-Akt inhibitor (GDC-0068), and we surprisingly found that GDC-0068 abrogated the inhibiting effects of Fasudil on cell autophagy and proliferation in the PUFs treated with TGF-beta. fasudil AKT serine/threonine kinase 1 Homo sapiens
6 SIGNIFICANCE: Fasudil regulated Akt/mTOR pathway mediated autophagy to hamper TGF-beta-mediated super-activation in PUFs, which supported that Fasudil might be an ideal candidate therapeutic agent for TUS treatment for clinical utilization. fasudil AKT serine/threonine kinase 1 Homo sapiens