We analyzed tumor necrosis factor-alpha -308 polymorphism in a total of 603 study participants: 293 elderly patients affected by acute myocardial infarction (STEMI and NSTEMI) and 310 healthy controls.
However, when subgroup analysis was performed according to the stages of MI, results indicated that there was a significant association between TNF-αG-308A polymorphism and the risk of acute MI.
We recently reported that the single nucleotide polymorphisms of the lymphotoxin-(LT)alpha gene, a member of the tumor necrosis factor (TNF) family, are closely related to acute myocardial infarction; however, the precise mechanism of LTalpha signaling in atherogenesis remains unclear.
However, the relationship between this polymorphism and susceptibility to AMI and the mechanism of TACE-TNF-α system regulation has poorly been studied.
We identified four genetic risk sets for acute myocardial infarction (AMI) from information on functional gene variants that favor inflammation or modulate cholesterol metabolism: IL6 -174 G/C, TNF-308 G/A, IL10 -1082 G/A, SERPINA3 -51 G/T, IFNG +874 T/A, HMGCR -911 C/A, and APOE epsilon2/3/4; 316 patients and 461 healthy subjects, all Italian.
Acute myocardial infarction in rats treated with only saline increased the myocardial concentration of tumor necrosis factor-alpha (TNF-alpha) from 6.9 +/- 0.8% to 51.3 +/- 4.6%, monocyte/macrophage chemoattractant protein (MCP-1) from 10.5 +/- 1.1% to 39.2 +/- 2.0%, monocyte inflammatory protein (MIP) from 10.6 +/- 1.6% to 23.1 +/- 1.5%, and interferon-gamma (INF-gamma) from 8.9 +/- 0.3% to 25.0 +/- 1.7% between 2 and 12 h after coronary occlusion in comparison with known controls (all p < 0.001).
We confirmed that the plasma sP‑selectin levels were increased in patients with obesity (particularly pericardial obesity) and hyperlipidemia, positively correlated with plasma tumor necrosis factor (TNF)‑α and strongly negatively correlated with adiponectin in all patients regardless of AMI status.
Tumor necrosis factor-stimulated gene-6 (TSG-6) is a 35-kDa glycoprotein that has been shown to exert anti-inflammatory effects in experimental models of arthritis, acute myocardial infarction, and acute cerebral infarction.
Because pentoxifylline inhibits platelet and neutrophil activation and reduces TNF-α, this study was performed to assess the potential benefit of pentoxifylline in the reduction of myocardial injury following acute MI.
Several studies suggest that tumor necrosis factor-related apoptosis inducing ligand (TRAIL) represents a very promising marker of prognosis in patients with acute myocardial infarction.
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).
To investigate the protective effect of tumor necrosis factor receptor (TNFR) gene modified mesenchymal stem cells (MSCs) transplantation against inflammation and cardiac dysfunction following acute myocardial infarction (AMI).
All together these results, indicating the relationship among genetically determined TNFα and FII production and increased levels of tissue damage markers of AMI, suggest that a complex genetic background, might be involved in susceptibility to AMI in young men influencing the extension and severity of the disease.
In the present study, western blotting was used to verified the expression of T lymphocyte CaSR and pathway proteins, including phosphorylated extracellular signal‑regulated kinase (P‑ERK)1/2 and phosphorylated c‑Jun N‑terminal kinase (P‑JNK), and used cytometric bead array to detect the secretion of interleukin (IL)‑4, IL‑6, IL‑10 and tumor necrosis factor (TNF)‑α in AMI onset, the results demonstrated that they were all increased.
We aimed to investigate changes in the levels of cytokines (IL-6, TNF-α and IL-10), miRNAs profiles (miR-146 and miR-155) and distribution of different monocyte subsets (CD14++CD16-, CD14++CD16+, CD14+CD16++) in the acute and post-healing phases of AMI.
The results of our study revealed that inflammatory cytokines IL-6 and TNF-<i>α</i> induce cardiac remodeling in rats after AMI; HMP improves cardiac function and ameliorates ventricular remodeling by downregulating the expression of IL-6 and TNF-<i>α</i> and further suppressing the ultrastructural changes of myocardial cells.
Treatment with dabigatran significantly inhibited the P65 of nuclear factor κB, tumor necrosis factor α, interleukin (IL)‑1β and IL‑6 activities and significantly enhanced the catalase and superoxide dismutase activities in the AMI rabbits.
The findings indicated that diminazene significantly reduced the levels of inflammatory factors including tumor necrosis factor‑α and interleukin‑6, suppressed the protein expression of cytochrome c oxidase subunit 2 (COX‑2) and inducible nitric oxide synthase (iNOS), and activated angiotensin‑converting enzyme 2 (ACE2), angiotensin II receptor type 1 (AT1R) and MAS1 proto‑oncogene, G protein‑coupled receptor (MasR) protein expression in AMI model rats.
Paired comparisons of subgroups with stable angina, unstable angina, and acute myocardial infarction (AMI) revealed significant variation in plasma levels of apoCIII, TNF-α and hs-CRP (P < 0.01), but not among subgroups with mild, moderate and severe stenosis (P > 0.05).
We investigated the relationship between pain during AMI and levels of circulating proinflammatory (tumor necrosis factor [TNF]-α, interleukin [IL]-6) and anti-inflammatory (IL-33 and tissue growth factor [TGF]-β1) cytokines.
The increased KIM-1 and NGAL expression levels after MI in the OLETF kidney were associated with upregulated expression of TLR1, TLR2, TLR4, MyD88, IL-6, TNF-α, chemokine (C-C motif) ligand 2, and transforming growth factor-β<sub>1</sub> and also with activation of p38 MAPK, JNK, and NF-κB.