PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24067190-11	2013	CONCLUSIONS: We conclude that irbesartan prevents ACE2 deficiency-mediated pathological hypertrophy and myocardial fibrosis in ACE2 mutant mice via activation of the PPARgamma signaling and suppression of the TGFbeta-CTGF-ERK signaling, resulting in attenuation of myocardial injury.	Irbesartan	30-40	angiotensin I converting enzyme (peptidyl-dipeptidase A) 2	Mus musculus	50-54	
29155324-0	2018	Angiotensin receptor blocker irbesartan reduces stress-induced intestinal inflammation via AT1a signaling and ACE2-dependent mechanism in mice.	Irbesartan	29-39	angiotensin I converting enzyme (peptidyl-dipeptidase A) 2	Mus musculus	110-114	
29155324-9	2018	Administration of irbesartan inhibited activation of stress-induced AT1 pathway to reduce intestinal ROS accumulation and inflammation, restored expression of ACE2/B0AT-1, activity of mTOR and p70S6K, dysbiosis and tryptophan metabolism.	Irbesartan	18-28	angiotensin I converting enzyme (peptidyl-dipeptidase A) 2	Mus musculus	159-163	
24067190-0	2013	Cardiac protective effects of irbesartan via the PPAR-gamma signaling pathway in angiotensin-converting enzyme 2-deficient mice.	Irbesartan	30-40	angiotensin I converting enzyme (peptidyl-dipeptidase A) 2	Mus musculus	81-112	
24067190-3	2013	We hypothesized that irbesartan would exert its protective effects on ACE2 deficiency-mediated myocardial fibrosis and cardiac injury via the PPARgamma signaling.	Irbesartan	21-31	angiotensin I converting enzyme (peptidyl-dipeptidase A) 2	Mus musculus	70-74	
24067190-9	2013	Intriguingly, treatment with irbesartan significantly reversed ACE2 deficiency-mediated pathological hypertrophy and myocardial fibrosis in Ace2(-/y) mice linked with enhancement of plasma Ang-(1-7) level and downregulation of AT1 receptor in heart.	Irbesartan	29-39	angiotensin I converting enzyme (peptidyl-dipeptidase A) 2	Mus musculus	63-67	
24067190-9	2013	Intriguingly, treatment with irbesartan significantly reversed ACE2 deficiency-mediated pathological hypertrophy and myocardial fibrosis in Ace2(-/y) mice linked with enhancement of plasma Ang-(1-7) level and downregulation of AT1 receptor in heart.	Irbesartan	29-39	angiotensin I converting enzyme (peptidyl-dipeptidase A) 2	Mus musculus	140-144	
24067190-11	2013	CONCLUSIONS: We conclude that irbesartan prevents ACE2 deficiency-mediated pathological hypertrophy and myocardial fibrosis in ACE2 mutant mice via activation of the PPARgamma signaling and suppression of the TGFbeta-CTGF-ERK signaling, resulting in attenuation of myocardial injury.	Irbesartan	30-40	angiotensin I converting enzyme (peptidyl-dipeptidase A) 2	Mus musculus	127-131	
19808375-7	2009	Treatment of Ace2(-)(/y)-MI mice with irbesartan, an AT1 receptor blocker, reduced nicotinamide-adenine dinucleotide phosphate oxidase activity, infarct size, MMP activation, and myocardial inflammation, ultimately resulting in improved post-MI ventricular function.	Irbesartan	38-48	angiotensin I converting enzyme (peptidyl-dipeptidase A) 2	Mus musculus	13-17	
22508831-9	2012	Thus, treatment with the AT(1)R blocker irbesartan and Ang 1-7 prevented the cardiac hypertrophy and improved cardiac remodeling in pressure-overloaded ACE2-null mice by suppressing NADPH oxidase and normalizing pathological signaling pathways.	Irbesartan	40-50	angiotensin I converting enzyme (peptidyl-dipeptidase A) 2	Mus musculus	152-156	
22693641-8	2012	Interestingly, daily treatment with AT1 receptor blocker irbesartan (50 mg/kg) significantly prevented Ang II-mediated aortic profilin-1 expression, inflammation, and peroxynitrite production in WT mice with enhanced ACE2 levels and the suppression of the Akt-ERK-eNOS signaling pathways.	Irbesartan	57-67	angiotensin I converting enzyme (peptidyl-dipeptidase A) 2	Mus musculus	217-221	
19650157-7	2009	One-year-old ace2 KO mice spontaneously developed an inflammatory cell infiltration and mild hepatic fibrosis that was prevented by treatment with irbesartan.	Irbesartan	147-157	angiotensin I converting enzyme (peptidyl-dipeptidase A) 2	Mus musculus	13-17	
16723697-4	2006	These structural and functional changes in the glomeruli of male ACE2 mutant mice were prevented by treatment with the angiotensin II type-1 receptor antagonist irbesartan.	Irbesartan	161-171	angiotensin I converting enzyme (peptidyl-dipeptidase A) 2	Mus musculus	65-69	
17499227-5	2007	The angiotensin II receptor-1 (AT1) blocker, irbesartan, prevented the dilated cardiomyopathy in aged Ace2(-/y) mutant mice, confirming a critical role of angiotensin II (Ang II)-mediated stimulation of AT1 receptors.	Irbesartan	45-55	angiotensin I converting enzyme (peptidyl-dipeptidase A) 2	Mus musculus	102-106