KLF2, Kruppel like factor 2, 10365

N. diseases: 132; N. variants: 3
Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0004153
Disease: Atherosclerosis
Atherosclerosis
0.100 Biomarker disease BEFREE Low-dose phloretin helped with lipid metabolism, and blocked the acceleration of atherosclerosis in STZ-induced diabetic mice since the early stage, which was diminished by KLF2 knockdown. 31791197 2020
CUI: C0004153
Disease: Atherosclerosis
Atherosclerosis
0.100 AlteredExpression disease BEFREE Simvastatin upregulated the reduced expression of Klf2 and Foxp1 in atherosusceptible vascular endothelium and alleviated vascular inflammation contributing to its inhibitory effect in atherosclerosis. 31318658 2019
CUI: C0004153
Disease: Atherosclerosis
Atherosclerosis
0.100 Biomarker disease BEFREE The KLF2 and NF-<i>κ</i>B may be potential therapeutic targets for interventions of inflammation associated with atherosclerosis. 30881601 2019
CUI: C0004153
Disease: Atherosclerosis
Atherosclerosis
0.100 AlteredExpression disease BEFREE MANTIS is tightly regulated by the transcription factors KLF2 and KLF4 and limits the ICAM-1 mediated monocyte adhesion to endothelial cells and thus potentially atherosclerosis development in humans. 31222221 2019
CUI: C0004153
Disease: Atherosclerosis
Atherosclerosis
0.100 Biomarker disease BEFREE This study demonstrates the characteristic impact of EVs from ox-LDL-treated and/or KLF2-transduced ECs on the monocyte/macrophage phenotype in vitro and in vivo.Q-PCR showed that both the atherosclerosis inducer ox-LDL and atheroprotective factor KLF2 regulated inflammation-associated microRNA-155 (miR-155) expression in human umbilical vein endothelial cells (HUVECs). 29465752 2018
CUI: C0004153
Disease: Atherosclerosis
Atherosclerosis
0.100 Biomarker disease BEFREE Our findings provide a novel mechanism for the well-established beneficial cardiovascular effects of TA and suggest that KLF2 could be a novel therapeutic target for atherosclerotic vascular disease. 28751752 2017
CUI: C0004153
Disease: Atherosclerosis
Atherosclerosis
0.100 Biomarker disease BEFREE These results demonstrate that SAHA has KLF2-dependent anti-inflammatory effects in endothelial cells and provide the proof of concept that KLF2 activation could be a promising therapeutic strategy for treating atherosclerosis. 29191808 2017
CUI: C0004153
Disease: Atherosclerosis
Atherosclerosis
0.100 Biomarker disease BEFREE Transplant of bone marrow from mice with KLF2-deficient DCs into Ldlr<sup>-/-</sup> mice aggravated atherosclerosis compared with control mice, most likely due to heightened vascular inflammation evidenced by increased DC presence within lesions, enhanced T cell activation and cytokine production, and increased cell death in atherosclerotic lesions. 27837103 2016
CUI: C0004153
Disease: Atherosclerosis
Atherosclerosis
0.100 AlteredExpression disease BEFREE In silico analysis of gene expression profiles from studies that assessed the effects of KLF2 overexpression in vitro and atherosclerosis in vivo on endothelial cells, identifies AQP1 as KLF2 downstream gene with elevated expression in the plaque-free vessel wall. 26717516 2015
CUI: C0004153
Disease: Atherosclerosis
Atherosclerosis
0.100 AlteredExpression disease BEFREE Expression of KLF4 in PBMCs positively correlates with cellular markers of immune activation, whereas KLF2 expression negatively correlates with markers of subclinical atherosclerosis in this HIV-infected population on ART. 26372274 2015
CUI: C0004153
Disease: Atherosclerosis
Atherosclerosis
0.100 AlteredExpression disease BEFREE Taken together, our results reveal that phosphorylation-dependent derepression of HDAC5 mediates flow-induced KLF2 and eNOS expression as well as flow anti-inflammation, and suggest that HDAC5 could be a potential therapeutic target for the prevention of atherosclerosis. 20042720 2010
CUI: C0004153
Disease: Atherosclerosis
Atherosclerosis
0.100 Biomarker disease BEFREE KLF2 is absent from low-shear, atherosclerosis-prone sites of the vascular tree but is induced by HMG-CoA reductase inhibitors (statins) in vitro. 16945356 2006