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A better understanding of neuroinflammation could open therapeutic avenues for abrogation of secondary cell death and behavioral symptoms that may mediate the progression of TBI.
In response to endothelial activation, monocytes and T-cells mediate the progression of atherosclerosis.
Differentially regulated pathways potentially mediate the progression from systemic inflammation to localised inflammatory-driven tissue damage.
The crosstalk between Kupffer cells and HSCs has been reported to mediate the progression of hepatic fibrosis.
Nonetheless, it seems very likely that additional pathogenic alterations instrumentally mediate the progression and dissemination of human HCC.
Furthermore, upregulation of bradykinin receptor has been described to mediate the progression of focal segmental glomerulosclerosis [ 45].
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ERS mediates the progression of ischemic cardiomyopathy.
Overall, further studies are required to establish the role of TLR9 in mediating the progression of SLE.
Dendritic cells (DCs) are the primary response cells mediating the progression from innate to adaptive immunity and the induction of self-tolerance [2], [3].
While the physiologic impact of cell fusion is not yet known, the increased incidence in an inflammatory and proliferative microenvironment suggests a potential role for cell fusion in mediating the progression of intestinal inflammatory diseases and cancer.
Chronic hypoxia mediates the progression of renal fibrosis, even from the early stages of CKD [ 16].
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