Adipocytokines such as tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), adiponectin, leptin, resistin along with peroxisome proliferator activated receptor-γ (PPAR-γ) are important mediators in glucose homeostasis in association with CD36 and can be used as markers for T2DM and atherosclerosis.
Hyperuricemia and artery atherosclerosis are closely associated and, as a classic inflammatory biomarker, tumor necrosis factor‑α (TNF‑α) has a direct role in atherogenesis.
Several lines of evidence support a key role for tumor necrosis factor-alpha (TNF-alpha), a potent immunomodulator and pro-inflammatory cytokine, in the development of atherosclerosis and in complications of CAD.
Through screening expression patterns of typical genes involved in atherosclerosis and foam cell generation, we could demonstrate that mRNA levels of cyclooxygenase-2, interleukin 1beta, and tumor necrosis factor-alpha were increased in a time- and dose-dependent manner in U937 macrophages treated with TCDD, like oxLDL, and that these changes accompanied significantly elevated levels of matrix-degrading metalloproteinases (MMP)-1, MMP-3, MMP-12, and MMP-13.
Proinflammatory cytokines, like interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha), are implicated in the development of atherosclerosis.
Transforming growth factor beta-activated kinase 1 (TAK1) plays a critical role in TNFα-induced atherosclerosis via endothelial nitric oxide (NO) synthase (eNOS) uncoupling and NO reduction.
Despite a great diversity among studies, the attributed health benefits of the MedDiet and its components, such as OO, could be explained by a transcriptomic effect on atherosclerosis, inflammation, and oxidative stress-related genes (i.e.ADRB2, IL7R, IFNγ, MCP1, TNFα).
Lymphotoxin alpha (LTA), one of the tumor necrosis factor family proteins, is an important proinflammatory cytokine and appears to play a putative role in the inflammatory process of atherosclerosis.
Our results suggested that though TNF-alphaG-238A and G-308A polymorphisms were not involved in the pathogenesis of type 2 DM, type 2 diabetic patients carrying TNFA-A or TNF-308*2 genotype might be more susceptible to diabetic complications such as atherosclerosis.
Moreover, miR-144-3p mimics (agomir) enhanced the expression of inflammatory factors, including IL-1β, IL-6 and TNF-α, in vivo and in vitro, inhibited cholesterol efflux in THP-1 macrophage-derived foam cells, decreased HDL-C circulation and impaired RCT in vivo, resulting in accelerated pathological progression of atherosclerosis in apoE-/- mice.
Proinflammatory cytokines, such as C-reactive protein, tumor necrosis factor alpha (TNFα), interleukins 1 and 6, that are markedly increased in RA, play a role in the acceleration of atherosclerosis as well as myocardial fibrosis development.
The role of TNF-α, TNF receptor 1 (TNFR1), and TNF receptor 2 (TNFR2), in Chlamydia pneumoniae (CPN)-induced atherosclerosis was studied using the high-fat diet-fed male C57BL/6J mouse model.
Compared with those in the NC group, the serum levels of interleukin-6 (IL-6), IL-10, IL-13 and tumor necrosis factor-α (TNF-α) in the AS group significantly increased (p<0.05).
The present study indicated that the mechanism underlying the effects of Tianxiangdan Granule on the prevention and treatment of atherosclerosis may be as follows: Tianxiangdan Granule may decrease the expression of the inflammatory cytokines IL‑1β and TNF‑α, and suppress activation of the NF‑κB p65 and p38 MAPK signaling pathways.