Gene | Score gda | Association Type | Type | Original DB | Sentence supporting the association | PMID | PMID Year | ||||
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0.530 | Biomarker | phenotype | RGD | Rescue treatment with a Rho-kinase inhibitor normalizes right ventricular function and reverses remodeling in juvenile rats with chronic pulmonary hypertension. | 20889845 | 2010 | ||||
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0.530 | Biomarker | phenotype | CTD_human | Gene expression of endothelin-1 and endothelin receptor a on monocrotaline-induced pulmonary hypertension in rats after bosentan treatment. | 20967148 | 2010 | ||||
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0.530 | Biomarker | phenotype | CTD_human | The correlation of changes in PVR and plasma ET-1 levels in responders suggests that high plasma ET-1 is a key mediator of poor response in PH secondary to MS, after iNO therapy. | 20929026 | 2010 | ||||
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0.530 | AlteredExpression | phenotype | LHGDN | [Assessment of plasma endothelin level measurement in systemic sclerosis]. | 17291632 | 2007 | ||||
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0.530 | AlteredExpression | phenotype | LHGDN | Hemodynamic and clinical correlates of endothelin-1 in chronic thromboembolic pulmonary hypertension. | 16864942 | 2006 | ||||
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0.530 | Biomarker | phenotype | LHGDN | Induction of apoptosis and endothelin-1 secretion in primary human lung endothelial cells by HIV-1 gp120 proteins. | 15979050 | 2005 | ||||
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0.530 | Biomarker | phenotype | CTD_human | Finally, we suggest that these observations may help to explain why patients with pulmonary hypertension experience exacerbations after taking indomethacin and that the newly introduced selective cyclooxygenase-2 inhibitors may increase endothelin-1 production in susceptible patients, leading to vascular remodeling and the development of pulmonary hypertension. | 12391278 | 2002 | ||||
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0.530 | Biomarker | phenotype | CTD_human | These results indicate that chronic fenfluramine exposure potentiates the pulmonary vasoconstrictor response to ET-1, and suggests that elevated levels of serotonin may <prime> the pulmonary circulation to become hyperreactive to other vasoactive substances possibly leading to the development of disease states such as primary pulmonary hypertension. | 9918753 | 1999 | ||||
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0.530 | Biomarker | phenotype | CTD_human | To explain the increase in potency it is speculated that during the development of pulmonary hypertension the mechanism whereby ET-1 and NA contract pulmonary arteries may change from one in which Ca2+ influx plays only a minor role to one in which Ca2+ influx predominates, although no direct evidence to support this speculation has yet been obtained. | 7549228 | 1994 |