PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
32307232-11	2020	Patients treated with ACEIs showed a progressive reduction in ACE levels to five years of follow-up (p=1.3E-02) and the zofenopril group recorded the highest ACE levels (p<1E-04).	aceis	22-27	angiotensin I converting enzyme	Homo sapiens	62-65
32712300-3	2020	The use of ACEIs/ARBs (RAAS inhibitors) regulates the renin-angiotensin-aldosterone system (RAAS) and may increase ACE2 expression.	aceis	11-16	angiotensin converting enzyme 2	Homo sapiens	115-119
32712300-5	2020	In this review, we summarize preclinical and clinical studies to investigate whether the use of ACEIs/ARBs increases ACE2 expression in animals or patients.	aceis	96-101	angiotensin converting enzyme 2	Homo sapiens	117-121
32307232-12	2020	CONCLUSIONS: This retrospective study investigated changes in ACE levels in patients with sarcoidosis treated or not treated with ACEIs.	aceis	130-135	angiotensin I converting enzyme	Homo sapiens	62-65
30825199-5	2019	All theses effects of AGE were reversed by treatment with ACEIs (captopril and enalapril), the NO donor S-nitroso-N-acetylpenicillamine (SNAP), and the PKG activator 8-para-chlorophenylthio-cGMPs (8-pCPT-cGMPs).	aceis	58-63	renin binding protein	Homo sapiens	22-25
32341442-3	2020	Given that angiotensin receptor blockers (ARBs) and an ACE inhibitor (ACEI) upregulated ACE2 expression in animal studies, the concern might arise regarding whether ARBs and ACEIs would increase the morbidity and mortality of COVID-19.	aceis	174-179	angiotensin I converting enzyme	Homo sapiens	55-58
32665962-4	2020	The concern is that the use of ACEIs and ARBs will increase the expression of ACE2 and increase patient susceptibility to viral host cell entry and propagation.	aceis	31-36	angiotensin converting enzyme 2	Homo sapiens	78-82
32611305-6	2020	Intravenous infusions of ACEIs and ARBs in experimental animals increase the number of ACE2 receptors.	aceis	25-30	angiotensin converting enzyme 2	Homo sapiens	87-91
32311651-5	2020	ACEIs and ARBs lead to a reduction in angiotensin II level by increasing the ACE2 level, thus they cause a low cytosolic pH.	aceis	0-5	angiotensinogen	Homo sapiens	38-52
32311651-5	2020	ACEIs and ARBs lead to a reduction in angiotensin II level by increasing the ACE2 level, thus they cause a low cytosolic pH.	aceis	0-5	angiotensin converting enzyme 2	Homo sapiens	77-81
32311651-6	2020	Increased cardiac ACE2 levels due to ACEIs and ARBs can trigger cardiac arrhythmias and myocarditis by causing the virus to easily enter the heart tissue.	aceis	37-42	angiotensin converting enzyme 2	Homo sapiens	18-22
27122684-7	2013	Likewise, among patients treated with at least ACEIs or ARBs and diuretics, the relative proportion of SPC use, in contrast to free combinations, increased markedly (from 10.8% to 54.2%, p = 0.005).	aceis	47-52	proline rich protein gene cluster	Homo sapiens	103-106
30825199-7	2019	The abilities of ACEIs and NO/PKG activation to inhibit AGE-induced hypertrophic growth were verified by the observation that captopril, enalapril, SNAP, and 8-pCPT-cGMPs decreased protein levels of fibronectin, p21 Waf1/Cip1 , and receptor for AGE.	aceis	17-22	renin binding protein	Homo sapiens	56-59
30825199-7	2019	The abilities of ACEIs and NO/PKG activation to inhibit AGE-induced hypertrophic growth were verified by the observation that captopril, enalapril, SNAP, and 8-pCPT-cGMPs decreased protein levels of fibronectin, p21 Waf1/Cip1 , and receptor for AGE.	aceis	17-22	fibronectin 1	Homo sapiens	199-210
30825199-7	2019	The abilities of ACEIs and NO/PKG activation to inhibit AGE-induced hypertrophic growth were verified by the observation that captopril, enalapril, SNAP, and 8-pCPT-cGMPs decreased protein levels of fibronectin, p21 Waf1/Cip1 , and receptor for AGE.	aceis	17-22	cyclin dependent kinase inhibitor 1A	Homo sapiens	212-225
30825199-7	2019	The abilities of ACEIs and NO/PKG activation to inhibit AGE-induced hypertrophic growth were verified by the observation that captopril, enalapril, SNAP, and 8-pCPT-cGMPs decreased protein levels of fibronectin, p21 Waf1/Cip1 , and receptor for AGE.	aceis	17-22	renin binding protein	Homo sapiens	245-248
30825199-8	2019	The results of the present study suggest that ACEIs significantly reduced AGE-increased ERK/JNK/p38 MAPK activation and renal tubular hypertrophy partly through enhancement of the NO/PKG pathway.	aceis	46-51	renin binding protein	Homo sapiens	74-77
30825199-8	2019	The results of the present study suggest that ACEIs significantly reduced AGE-increased ERK/JNK/p38 MAPK activation and renal tubular hypertrophy partly through enhancement of the NO/PKG pathway.	aceis	46-51	mitogen-activated protein kinase 1	Homo sapiens	88-91
30825199-8	2019	The results of the present study suggest that ACEIs significantly reduced AGE-increased ERK/JNK/p38 MAPK activation and renal tubular hypertrophy partly through enhancement of the NO/PKG pathway.	aceis	46-51	mitogen-activated protein kinase 8	Homo sapiens	92-95
30825199-8	2019	The results of the present study suggest that ACEIs significantly reduced AGE-increased ERK/JNK/p38 MAPK activation and renal tubular hypertrophy partly through enhancement of the NO/PKG pathway.	aceis	46-51	protein kinase cGMP-dependent 1	Homo sapiens	183-186
25239727-8	2014	Preclinical studies targeting either activity or production of ET-1 - utilizing ERAs, ARBs, or ACEIs, respectively - have demonstrated that partial regression of aging-associated changes in vasculature and kidney is possible.	aceis	95-100	endothelin 1	Homo sapiens	63-67
23733546-7	2013	Prevention of diabetes-induced changes in ACE expression and Na(+) /K(+) -ATPase activity could be a new explanation of the renoprotective effects of ACEIs and ARBs.	aceis	150-155	angiotensin I converting enzyme	Rattus norvegicus	42-45
25962494-11	2015	In a multivariate model, after adjusting for ACEIs/ARBs discontinuation/dose reduction, NSAIDs use and change in DBP, an increase in SBP at time 1 remained significantly associated with increments in GFR on follow-up (estimate = 0.20, p = 0.01).	aceis	45-50	selenium binding protein 1	Homo sapiens	133-136
27122684-9	2013	The increase in patients taking SPCs came mostly from the naive SPC prescription group (from 2.3% in 2002 to 28.8% in 2007 among all patients treated with ACEIs or ARBs and thiazide diuretics, p = 0.003).	aceis	155-160	proline rich protein gene cluster	Homo sapiens	32-35
21241234-7	2011	The long lasting direct renin inhibitor aliskiren, acting at the first and rate limiting step of the RAAS cascade, prevents the reactive increase in PRA when combined with ACEIs, ARBs or diuretics.	aceis	172-177	renin	Homo sapiens	24-29
11217909-11	2001	These findings provide further evidence of a link between ACEI-induced cough and I/D polymorphism of the ACE gene and suggest that ACEIs induce cough by modulating the tissue level of bradykinin.	aceis	131-136	kininogen 1	Homo sapiens	184-194
20329582-4	2010	Administration of ACEIs and ARBs interrupts physiological feedback for renal renin release and leads to reactive elevation of circulating active renin and greater production of angiotensin I and angiotensin II with subsequent return of aldosterone secretion to the pre-treatment levels ("escape" phenomenon).	aceis	18-23	renin	Homo sapiens	77-82
20329582-4	2010	Administration of ACEIs and ARBs interrupts physiological feedback for renal renin release and leads to reactive elevation of circulating active renin and greater production of angiotensin I and angiotensin II with subsequent return of aldosterone secretion to the pre-treatment levels ("escape" phenomenon).	aceis	18-23	renin	Homo sapiens	145-150
20329582-4	2010	Administration of ACEIs and ARBs interrupts physiological feedback for renal renin release and leads to reactive elevation of circulating active renin and greater production of angiotensin I and angiotensin II with subsequent return of aldosterone secretion to the pre-treatment levels ("escape" phenomenon).	aceis	18-23	angiotensinogen	Homo sapiens	177-190
20329582-4	2010	Administration of ACEIs and ARBs interrupts physiological feedback for renal renin release and leads to reactive elevation of circulating active renin and greater production of angiotensin I and angiotensin II with subsequent return of aldosterone secretion to the pre-treatment levels ("escape" phenomenon).	aceis	18-23	angiotensinogen	Homo sapiens	195-209
15384808-10	2004	We conclude that treatment with ACEIs and ARBs induces erythropoietin resistance in patients on CAPD.	aceis	32-37	erythropoietin	Homo sapiens	55-69
12473875-2	2002	The aim of our study was to compare chemically different ACEIs regarding their ability to modulate left ventricular and media hypertrophy, ACE activity and plasma endothelin-1 concentrations in spontaneously hypertensive rats (SHRs).	aceis	57-62	endothelin 1	Rattus norvegicus	163-175
9066005-4	1997	Bradykinin was infused in seventeen hypertensive patients randomized to treatment with the ACEIs captopril and quinapril or with placebo.	aceis	91-96	kininogen 1	Homo sapiens	0-10
33768439-5	2021	Many researchers have voiced concerns that the use of ACEIs and ARBs may increase tissue ACE2 levels.	aceis	54-59	angiotensin converting enzyme 2	Homo sapiens	89-93
33768439-10	2021	Further studies are required to investigate the effect of ACEIs and ARBs on ACE2 expression and COVID-19.	aceis	58-63	angiotensin converting enzyme 2	Homo sapiens	76-80
34265036-5	2022	The effect of ACEIs on the tissue and plasma levels of bradykinin and on nitric oxide production and bioavailability is specific to the mechanism of action of ACEIs; it could account for the different effects of ACEIs and ARBs on endothelial function, atherogenesis and fibrinolysis.	aceis	14-19	kininogen 1	Homo sapiens	55-65
34265036-5	2022	The effect of ACEIs on the tissue and plasma levels of bradykinin and on nitric oxide production and bioavailability is specific to the mechanism of action of ACEIs; it could account for the different effects of ACEIs and ARBs on endothelial function, atherogenesis and fibrinolysis.	aceis	159-164	kininogen 1	Homo sapiens	55-65
34265036-5	2022	The effect of ACEIs on the tissue and plasma levels of bradykinin and on nitric oxide production and bioavailability is specific to the mechanism of action of ACEIs; it could account for the different effects of ACEIs and ARBs on endothelial function, atherogenesis and fibrinolysis.	aceis	212-217	kininogen 1	Homo sapiens	55-65
33674289-5	2021	The use of antiproteinuric drugs, such as anti-ACE inhibitors (ACEis) and hydroxyurea, should be considered in early stages.	aceis	63-68	angiotensin I converting enzyme	Homo sapiens	47-50
34268008-2	2021	However, no guidelines have clearly indicated which kinds of renin angiotensin system blockade therapies (ACEIs or ARBs or their combination) in patients with IgAN result in a greater reduction in proteinuria and a better preservation of kidney function.	aceis	106-111	renin	Homo sapiens	61-66
33290594-6	2021	ACEIs and ARBs may increase the amount of ACE-2 formation and, theoretically, increase the risk of SARS-CoV-2 entry into cells, thus inducing inflammation [2].	aceis	0-5	angiotensin converting enzyme 2	Homo sapiens	42-47
33426364-5	2021	The CVD drugs ACEIs and ARBs, as well as the T2D drugs GLP-1R agonists, were shown to activate angiotensin-converting enzyme 2 (ACE2) expression in experimental animals.	aceis	14-19	angiotensin converting enzyme 2	Homo sapiens	95-126
33426364-5	2021	The CVD drugs ACEIs and ARBs, as well as the T2D drugs GLP-1R agonists, were shown to activate angiotensin-converting enzyme 2 (ACE2) expression in experimental animals.	aceis	14-19	angiotensin converting enzyme 2	Homo sapiens	128-132
33475077-3	2021	OBJECTIVE: The purpose of this review is to discuss the existing evidence on the interaction between COVID-19 infection, ACE2 and ACEIs or ARBs and to examine the main implications for clinical practice.	aceis	130-135	angiotensin converting enzyme 2	Homo sapiens	121-125