Last, PNA5 treatment decreased VCID/HF-induced activation of brain microglia/macrophages and inhibited circulating tumor necrosis factor <i>α</i>, interleukin (IL)-7, and granulocyte cell-stimulating factor serum levels while increasing that of the anti-inflammatory cytokine IL-10.
So far, it has been found that inflammatory cytokines associated with the heart failure mechanism include TNF-<i>α</i>, IL-6, IL-8, IL-10, IL-1<i>α</i>, IL-1<i>β</i>, IL-2, TGF-<i>β</i>, and IFN-<i>γ</i>.
Inflammation is a central process in the pathophysiology of heart failure (HF), but trials targeting tumour necrosis factor (TNF)-α were largely unsuccessful.
In this review, we describe available data on the occurrence of adverse events associated with TNF inhibitor treatment in ankylosing spondylitis, including serious adverse events, infections, serious infections, tuberculosis, opportunistic infections, hepatitis B reactivation, malignancies, laboratory test abnormalities, autoimmune diseases, paradoxical adverse events, and heart failure.
The protective and anti-inflammatory effects of TNFR2 may explain why TNF inhibitors failed to be effective in diseases such as heart failure or multiple sclerosis, where TNF has been strongly implicated as a driving force.
A functional analysis of T cells from patients with acute HF revealed that the CD4<sup>+</sup>CD57<sup>+</sup> T cell population exhibited a higher frequency of IFN-γ- and TNF-α- producing cells compared to the CD4<sup>+</sup>CD57<sup>-</sup> T cell population.
Patients with MI and HF had reduced serum irisin, LVEF, and HDL-C and higher levels of BMI, WHR, SBP, DBP, troponin-I, creatine kinase-MB (CK-MB), TNF-α, TC, TGs, and LDL-C compared with control.
Studies have shown co-relationship between severity of heart failure and levels of the proinflammatory cytokine TNFα and one of its secondary mediators interleukin-6 (IL-6), suggesting their potential as biomarkers.
In this review, we explore the emerging role of tumor necrosis factor receptor-associated factor 6 (TRAF6)-nuclear factor kappa B (NF-κB) signaling axis in atherosclerosis, ischemic heart disease, pathologic cardiac hypertrophy or heart failure, myocarditis, and sepsis-induced cardiomyopathy.
In the present study, we showed anti-inflammatory effects of liraglutide treatment, reflected in reductions in levels of TNF-α and MR-proADM, while the reduction in MR-proANP levels may represent a clinically relevant benefit with regard to heart failure.
Renal sympathetic denervation improves myocardial apoptosis in rats with isoproterenol-induced heart failure by downregulation of tumor necrosis factor-α and nuclear factor-κB.
Despite these well-described observations, less is known about the mechanistic underpinnings of proinflammatory cytokines especially TNFα in pathogenesis of HF.
After adjusting for eGFR, albuminuria, and other traditional cardiovascular risk factors, anemia (1.37, 95% CI 1.09, 1.72, <i>P</i>=0.006), insulin resistance (1.16, 95% CI 1.04, 1.28, <i>P</i>=0.006), hemoglobin A1c (1.27, 95% CI 1.14, 1.41, <i>P</i><0.001), interleukin-6 (1.15, 95% CI 1.05, 1.25, <i>P</i>=0.002), and tumor necrosis factor-α (1.10, 95% CI 1.00, 1.21, <i>P</i>=0.05) were all significantly and directly associated with incidence of heart failure.
We will analyze the role of some receptor mediated signaling pathways such as natriuretic peptides, mediators of glycogen synthase kinase 3 and ERK1/2 pathways, beta-adrenergic receptor subtypes and relaxin receptor signaling mechanisms, TNF/TNF receptor family and TWEAK/Fn14 axis, and some micro-RNAs as candidate target pathways in pathogenesis of heart failure.