Gene | Score gda | Association Type | Type | Original DB | Sentence supporting the association | PMID | PMID Year | ||||
---|---|---|---|---|---|---|---|---|---|---|---|
|
0.070 | AlteredExpression | phenotype | BEFREE | Therefore, we conclude that PM2.5 exposure induces MAPK/AP-1 cascade activation, which contributes to AT1R upregulation and vascular endothelial dysfunction. | 30529618 | 2019 | ||||
|
0.070 | GeneticVariation | phenotype | BEFREE | AGTR1 A1166C variant affects liver disease, insulin resistance, and endothelial dysfunction in NAFLD, at least in part by modulating adipokine, chemokine, and pro-inflammatory cell activation in response to fat ingestion. | 30920415 | 2019 | ||||
|
0.070 | AlteredExpression | phenotype | BEFREE | We conclude that interference with PPAR-γ in the endothelium produces endothelial dysfunction in the cerebral circulation in response to low salt-mediated activation of the endogenous renin-angiotensin system, mediated at least in part, through AT1 receptor activation and perturbed redox homeostasis. | 30354810 | 2018 | ||||
|
0.070 | Biomarker | phenotype | BEFREE | Mechanistically, the angiotensin II type 1 receptor was found to mediate 6-OHDA-induced endothelial dysfunction. | 29048735 | 2017 | ||||
|
0.070 | GeneticVariation | phenotype | BEFREE | The purpose of this study was to investigate the role of angiotensin type 1 receptor (AT1R) A1166C gene polymorphisms in the development of endothelial dysfunction and ISR after PCI. | 26261635 | 2015 | ||||
|
0.070 | GeneticVariation | phenotype | BEFREE | An increasing body of evidence suggests that different genetic factors, such as angiotensin-converting enzyme (ACE) I/D, angiotensin II type-1 receptor (AT1R) A1166C, methylenetetrahydrofolate reductase (MTHFR) C677T and ENOS G894T variants are associated with an endothelial dysfunction (ED). | 17504188 | 2007 | ||||
|
0.070 | Biomarker | phenotype | BEFREE | These findings suggest that the Ang II-AT(1) receptors pathway potentially are involved in OSAS and VEGF-induced vascularity and that endothelial dysfunction might be linked to this change in Ang II activity within leukocytes of OSAS patients. | 16085213 | 2005 |