TNF, tumor necrosis factor, 7124

N. diseases: 2724; N. variants: 31
Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 Biomarker disease BEFREE Further experiment indicated that SAL treatment reduced inflammatory factors such as IL-1β, IL-6, and TNF-α and decreased tunnel-positive cells and pro-apoptotic Bax after MI. 31811327 2019
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 Biomarker disease BEFREE We further evaluated the inflammation, fibrosis of left atria (LA), and related signal pathways by RT-PCR, Western blot, and staining analysis.Compared to the MI group, fisetin treatment improved cardiac function, inhibited macrophage recruitment into the LA and production of IL-1β and TNF-α, and attenuated adverse atrial fibrosis following acute myocardial infarction (AMI). 31666455 2019
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 AlteredExpression disease BEFREE Furthermore, pretreated group showed decreased activation of TNF-α, Caspase-3 activity along with reduction in the myocardial infarct size. 31630586 2019
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 AlteredExpression disease BEFREE The immunohistochemical staining results showed that IL-6 knockout could lower the MI-induced high expression of TNF-α (p<0.05), and Masson's trichrome staining indicated that IL-6 knockout could also repress the degree of cardiac fibrosis. 31364133 2019
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 Biomarker disease BEFREE C1q/tumor necrosis factor-related protein-3-engineered mesenchymal stromal cells attenuate cardiac impairment in mice with myocardial infarction. 31296837 2019
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 AlteredExpression disease BEFREE Dietary supplementation with flaxseed, ALA or SDG before and after the induction of the MI significantly reduced the incidence of arrhythmias and resulted in significantly smaller infarct size, less left ventricle dilation, and decreased myocardial fibrosis and tumor necrosis factor-α levels compared to the control MI group. 31284167 2019
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 Biomarker disease BEFREE The MI group produced a significant increase in myocardial infarct size, serum cardiac biomarkers (LDH and CK-MB), proinflammatory cytokines (TNF-α and IL-6), and MDA levels, and a significant decrease in SOD level compared with the sham group. 31280453 2019
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 Biomarker disease BEFREE Compared with control group, the levels of heart rate, left ventricular end-diastolic pressure, TNF-α, and IL-6 were increased in each group of rats with MI (all p < 0.05), while the levels of systolic blood pressure, diastolic blood pressure, mean arterial pressure, left ventricular systolic pressure, and IL-10 were significantly decreased (all p < 0.05). 31218464 2019
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 Biomarker disease BEFREE CCNP was more efficient than CC in limiting the increase in inflammatory cytokine levels (such as TNF-<i>α</i>, IL-6, IL-1<i>α</i>, IL-1<i>β</i>, MCP-1, and RANTES) after MI. 31205590 2019
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 Biomarker disease BEFREE Inflammation is a key factor in atherosclerosis, including endothelial function, plaque stabilization and post infarct remodeling; thus, inhibition of TNF-α may affect the inflammatory burden and plaque vulnerability leading to less cardiovascular events and myocardial infarctions. 31059840 2019
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 AlteredExpression disease BEFREE This study aimed to assess serum irisin level in myocardial infarction (MI) with or without heart failure (HF) and the possible relation between irisin and cardiac markers, tumor necrosis factor-α (TNF-α) and lipid profile. 30958967 2019
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 Biomarker disease BEFREE C1q/TNF-related protein-9 promotes macrophage polarization and improves cardiac dysfunction after myocardial infarction. 30953351 2019
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 AlteredExpression disease BEFREE The expression of IL-6, TNF-α, and inflammatory related molecules ICAM-1, VCAM-1, MMP-2 and -9, nuclear NF-kB, and iNOS, were elevated in MI-V. 30642049 2019
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 Biomarker disease BEFREE Adult male wild-type C57BL/6 mice, Foxp3-diphtheria toxin receptor transgenic mice, and tumor necrosis factor (TNF) α receptor-1 (TNFR1)<sup>-</sup><sup>/-</sup> mice underwent nonreperfused myocardial infarction to induce HF or sham operation. 30586716 2019
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 AlteredExpression disease BEFREE Phospholipase D1 is a regulator of tumor necrosis factor-α expression and release upon LPS-induced sepsis and following myocardial infarction (MI). 30555342 2018
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 PosttranslationalModification disease BEFREE Atorvastatin can improve cardiac remodeling after myocardial infarction in rats, which may be associated with its inhibition of p38 phosphorylation and its decrease of TNF-α expression. 30116330 2018
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 Biomarker disease BEFREE Enzyme-linked immunosorbent assay (ELISA) analysis showed that QLQX significantly reduced the levels of angiotensin II (AngII), brain natriuretic peptides (BNP), creatinine (CRE), cystatin C (CysC), tumor necrosis factor (TNF)-α, interleukin (IL)-6, microalbuminuria (MAU), and neutrophil gelatinase-associated lipocalin (NGAL) in plasma induced by myocardial infarction. 30068867 2018
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 Biomarker disease BEFREE S100A8/A9 promotes MMP-9 expression in the fibroblasts from cardiac rupture after myocardial infarction by inducing macrophages secreting TNFα. 29949169 2018
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 AlteredExpression disease BEFREE Gambogic acid suppressed the activation of interleukin (IL)-6 and tumor necrosis factor-α, and increased IL-10 levels in MI rats. 29434760 2018
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 Biomarker disease BEFREE Using iRhom2-deficient mice, which lack myeloid-specific shedding of TNF-α, we reveal increased macrophages (MΦs) that were skewed towards a more proinflammatory (M1) state at day 4, followed by more reparative, antiinflammatory (M2) state at day 7 after myocardial infarction (MI). 29415889 2018
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 Biomarker disease BEFREE In vivo, echocardiography was performed on rats with induced MI after their treatment with TNF-α and hypoxia-induced secretome. 29258676 2018
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 AlteredExpression disease BEFREE Moreover, S+MI group, but not S alone, showed a significant increase in the expression of connective tissue growth factor (CTGF) and fibrotic proteins fibronectin (FN) and <i>α</i>-smooth muscle actin (SMA), in comparison to controls, in addition to a significant increase in mRNA levels of IL-6 and TNF-<i>α</i> inflammatory markers. 29177025 2017
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 Biomarker disease BEFREE On the other hand, p21, S100A4 and TNF-α increased in the stromal fibroblasts of tissue from old myocardial infarctions. 28721450 2017
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 AlteredExpression disease BEFREE The MI group showed higher levels of cardiac TNF-α compared to the MIL and MIT groups. 28599197 2017
CUI: C0027051
Disease: Myocardial Infarction
Myocardial Infarction
0.600 Biomarker disease BEFREE The purpose of this study was to find out the possible association of modulation in NK cell, TNK cells, T cells, B cells, and tumor necrosis factor alpha (TNF-α) in CAD patients and various forms of myocardial infarction. 28414590 2017