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In view of lower bilirubin and higher hs-CRP levels in MetS our findings support the possibility that lower bilirubin could be implicated in enhanced low-grade systemic inflammation in MetS.
Depletion of tryptophan has also been shown to lead to stabilization of IL-6 and IL-8 mRNA, resulting in increased IL-6 and IL-8 responses that were proposed to be implicated in enhanced inflammatory responses to bacterial challenges after a viral infection [ 30].
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So far, only CD23 has been implicated in enhanced IL-4 dependent antibody shuttling through the intestinal epithelium [22], [23].
For example, the mtDNA 10398A polymorphism is implicated in enhanced ROS production, and was found to be a risk factor for breast cancer and esophageal cancer in Indian patients, and for invasive breast cancer in African-American women [4], [15].
TAM expression of IL-8 and a number of molecules, such as VEGF and TNF-α, have been implicated in enhanced angiogenesis [5], [62], while TAM-produced CCL18 can recruit naïve T cells to the microenvironment dominated by TAMs for possible T cell anergy [5].
Like in the case of VPS35, its deficiency has been implicated in enhanced Aβ production and AD pathogenesis [ 34].
Another TRP channel that has been implicated in enhanced motility and metastasis of cancer cells is TRPM7 channel.
hs-CRP is inversely related to bilirubin, suggesting that low bilirubin is implicated in enhanced low-grade systemic inflammation.
Furthermore, hERG expression is implicated in enhanced cell proliferation, invasiveness, lymph node dissemination, and reduced cell differentiation and prognosis.
These proteins have been implicated in enhanced tumorigenesis, invasion and metastasis thus targeting them could reap further therapeutic rewards [ 15– 15].
Therefore, as expected, activation of EGFR signaling in vascular SMCs is implicated in enhanced neointima formation observed in Mig-6 knockout mice.
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