PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33416889-5	2021	Paricalcitol treatment reduced renal collagen I and renal interstitial fibrosis by decreasing the activation of the renin-angiotensin-aldosterone system through renal changes in renin, ATR1 and ATR2 mRNAs levels and renal inflammation by decreasing renal inflammatory leukocytes (CD45), ADAM17 mRNA, TGF-beta mRNA and protein and maintaining E-cadherin mRNA levels.	paricalcitol	0-12	transforming growth factor alpha	Homo sapiens	300-308	
26064952-10	2015	Preincubation with the VDRA paricalcitol inhibited aldosterone-induced EGFR transactivation, TGF-alpha/ADAM-17 gene upregulation, and downstream mechanisms, including proinflammatory factors overexpression.	paricalcitol	28-40	transforming growth factor alpha	Homo sapiens	93-102	
26064952-11	2015	In conclusion, our data suggest that the anti-inflammatory actions of paricalcitol in tubular cells could depend on the inhibition of TGF-alpha/ADAM17/EGFR pathway in response to aldosterone, showing an important mechanism of VDRAs action.	paricalcitol	70-82	transforming growth factor alpha	Homo sapiens	134-143