INT70789

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Context Info
Confidence 0.48
First Reported 1997
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 26
Total Number 27
Disease Relevance 16.39
Pain Relevance 2.18

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

Golgi apparatus (Agtrap) endoplasmic reticulum (Agtrap) plasma membrane (Agtrap)
Anatomy Link Frequency
retina 3
neurons 2
neuronal 1
cardiomyocyte 1
vasculature 1
Agtrap (Mus musculus)
Pain Link Frequency Relevance Heat
tolerance 120 99.16 Very High Very High Very High
Kinase C 27 90.24 High High
agonist 18 85.04 High High
ischemia 16 85.04 High High
anesthesia 18 84.24 Quite High
Catecholamine 2 83.96 Quite High
beta blocker 3 83.16 Quite High
bradykinin 34 82.96 Quite High
Pseudotolerance 12 82.48 Quite High
Inflammatory response 9 81.52 Quite High
Disease Link Frequency Relevance Heat
Coronary Artery Disease 30 99.88 Very High Very High Very High
Apoptosis 102 99.68 Very High Very High Very High
Metastasis 52 99.68 Very High Very High Very High
Cardiovascular Disease 31 99.68 Very High Very High Very High
Cancer 243 99.24 Very High Very High Very High
Diabetes Mellitus 1049 99.08 Very High Very High Very High
Colon Cancer 140 98.96 Very High Very High Very High
Immunotherapy Of Cancer 4 98.08 Very High Very High Very High
Malignant Neoplastic Disease 4 97.72 Very High Very High Very High
Stress 86 97.12 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
AT1R blockade in vivo.
Negative_regulation (blockade) of AT1R
1) Confidence 0.48 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.74 Pain Relevance 0.03
In contrast, AT1R blockade did not affect the physiologic level of synatophysin mRNA or protein in the nondiabetic retina (data not shown).


Negative_regulation (blockade) of AT1R in retina
2) Confidence 0.48 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.48 Pain Relevance 0.04
Collectively, our present data show the possibility of AT1R blockade as a novel therapeutic strategy for neuronal dysfunction in vision-threatening diabetic retinopathy.



Negative_regulation (blockade) of AT1R in neuronal associated with diabetic retinopathy
3) Confidence 0.48 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.44 Pain Relevance 0
Importantly, AT1R blockade significantly improved these functional parameters in the diabetic retina to the normal levels observed in nondiabetic controls (Fig. 2).
Negative_regulation (blockade) of AT1R in retina associated with diabetes mellitus
4) Confidence 0.35 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.82 Pain Relevance 0
Diabetes-induced visual dysfunction was suppressed by AT1R blockade.
Negative_regulation (blockade) of AT1R associated with diabetes mellitus
5) Confidence 0.35 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.87 Pain Relevance 0
In contrast, AT1R blockade did not attenuate the baseline level of retinal pERK in nondiabetic mice (data not shown).


Negative_regulation (blockade) of AT1R
6) Confidence 0.35 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.82 Pain Relevance 0
Consistently, ERK phosphorylation, enhanced in 4-week diabetic mice (P < 0.01), was significantly (P < 0.01) attenuated by AT1R blockade with telmisartan or valsartan to the level equivalent with that in nondiabetic mice (Fig. 1D and E).
Negative_regulation (blockade) of AT1R associated with diabetes mellitus
7) Confidence 0.35 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.77 Pain Relevance 0
AT1R blockade significantly reversed diabetes-induced electroretinography changes and reduction of synaptophysin protein, but not mRNA, levels in the diabetic retina.
Negative_regulation (blockade) of AT1R in retina associated with diabetes mellitus
8) Confidence 0.35 Published 2008 Journal Diabetes Section Abstract Doc Link PMC2494692 Disease Relevance 0.55 Pain Relevance 0
Reasonably, the present ERG findings, in concert with our recent data on AT1R expression in the inner retinal neurons (14), the cellular origins of OPs, suggest that the functional recovery of the diabetic inner retina was attributable in part to the direct effect of AT1R blockade on the inner retinal neurons.
Negative_regulation (blockade) of AT1R in neurons associated with diabetes mellitus
9) Confidence 0.35 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.87 Pain Relevance 0.05
Similarly, the implicit time of OP2 and OP3, prolonged in 4-week diabetic mice, was significantly (P < 0.05 for both) recovered by AT1R blockade to the normal level (Fig. 2A and C).
Negative_regulation (blockade) of AT1R associated with diabetes mellitus
10) Confidence 0.35 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.68 Pain Relevance 0.03
The currently observed suppression of synaptophysin decrease by AT1R blockade (Fig. 3) is likely to rescue the activity of the AT1R-bearing inner retinal neurons, leading to the improvement of OP changes (Fig. 2).
Negative_regulation (blockade) of AT1R in neurons
11) Confidence 0.35 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.46 Pain Relevance 0.09
In agreement with the in vivo data (Fig. 3), in vitro application with angiotensin II significantly (P < 0.01) reduced synaptophysin protein (Fig. 4A and B), but not mRNA (Fig. 4C), levels in a posttranscriptional manner, which were significantly (P < 0.05 for all) reversed by AT1R blockade with telmisartan, valsartan, or shRNA for AT1R knockdown (Fig. 4A, B, and D–F).
Negative_regulation (knockdown) of AT1R
12) Confidence 0.35 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.20 Pain Relevance 0
This is consistent with the assumption that A1 receptor blockade mediates these effects.
Negative_regulation (blockade) of A1 receptor
13) Confidence 0.32 Published 2005 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 15590766 Disease Relevance 0.48 Pain Relevance 0.12
ANG II activation of the AT1R is associated with VEGF secretion and tumour angiogenesis is suppressed following AT1R blockade [23,29].
Negative_regulation (blockade) of AT1R associated with cancer
14) Confidence 0.21 Published 2010 Journal Cancer Cell Int Section Body Doc Link PMC2902462 Disease Relevance 1.31 Pain Relevance 0.08
While AT1R blockade has been extensively studied, the potential of targeting the antagonistically acting AT2R in cancer has not been investigated.
Negative_regulation (blockade) of AT1R associated with cancer
15) Confidence 0.21 Published 2010 Journal Cancer Cell Int Section Abstract Doc Link PMC2902462 Disease Relevance 1.04 Pain Relevance 0.04
The AT2R generally exerts actions antagonistic to the AT1R including inhibition of proliferation and angiogenesis [9,10] and promotion of apoptosis [11] and while AT1R blockade has been extensively studied in the context of cancer treatment, the potential of targeting the AT2R in cancer has not been investigated.
Negative_regulation (blockade) of AT1R associated with cancer, apoptosis and immunotherapy of cancer
16) Confidence 0.21 Published 2010 Journal Cancer Cell Int Section Body Doc Link PMC2902462 Disease Relevance 1.16 Pain Relevance 0.10
The RAS is now known to contribute to the regulation of tumour growth in several types of malignancy, but to date most research has focused on the inhibitory potential of blocking the classical RAS pathway, namely AT1R blockade or ACE inhibition [20-23].
Negative_regulation (blockade) of AT1R associated with malignant neoplastic disease and cancer
17) Confidence 0.21 Published 2010 Journal Cancer Cell Int Section Body Doc Link PMC2902462 Disease Relevance 0.91 Pain Relevance 0.03
Our results are in accordance with previous studies showing that cardiac remodeling in mice with global (not cardiomyocyte specific) GC-A disruption is markedly inhibited by genetic or pharmacological blockade of the AT1 receptor [27].
Negative_regulation (blockade) of AT1 receptor in cardiomyocyte
18) Confidence 0.14 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0.18 Pain Relevance 0.03
Blockade of AT-1 receptor significantly improved flow-mediated dilation (FMD) of the brachial artery, while no changes in the coronary district were observed (Warnholtz et al 2006).
Negative_regulation (Blockade) of AT-1 receptor in brachial artery
19) Confidence 0.05 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2464748 Disease Relevance 0.85 Pain Relevance 0.06
The hypothesis that the blockade of AT-1 receptor may exert a protective effect on vasculature was also tested in a study that compared equihypotensive doses of irbesartan and amlodipine in apolipoprotein E-null mice, rendered diabetic by streptozotocin.
Negative_regulation (blockade) of AT-1 receptor in vasculature associated with diabetes mellitus and disorder of lipid metabolism
20) Confidence 0.05 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2464748 Disease Relevance 0.55 Pain Relevance 0.04

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