PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33373654-0	2021	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	24-31	transforming growth factor alpha	Homo sapiens	44-52	
33373654-1	2021	AIMS: Transforming growth factor-beta (TGF-beta) mediated super-activation of urethra fibroblasts contributes to the progression of traumatic urethral stricture (TUS), and the Rho-associated kinase inhibitors, Fasudil, might be a novel therapeutic agent for TUS, but the underlying mechanisms had not been studied.	fasudil	210-217	transforming growth factor alpha	Homo sapiens	39-47	
33373654-6	2021	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	191-198	transforming growth factor alpha	Homo sapiens	13-21	
33373654-7	2021	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	150-157	transforming growth factor alpha	Homo sapiens	219-227	
33373654-8	2021	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	14-21	transforming growth factor alpha	Homo sapiens	78-86