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رونویسی
Attempts to inhib- it the inflammatory M1-like macrophage phenotype, including blocking activity of inflammatory cytokines and transcription factors involved in inducing this phenotype, have been investigated for the treatment of in- flammatory tissue diseases.
Finally, nanoparticle delivery of siRNA against the transcription factor in- sulin response factor (IRF)-5, which has been associated with the M1-like phenotype, reduced expression of inflammatory genes in macrophages, reduced protease activity and promoted the resolution of inflammation after myocardial infarction in mice, with reduced subsequent left ventric- ular dilation [81].
, In vivo silencing of the transcription factor IRF5 reprograms the macrophage pheno- type and improves infarct healing, J.
, Macrophage transcriptional profile identifies lipid catabolic pathways that can be therapeutical- ly targeted after spinal cord injury, J.
This signaling pathway activates the transcription factor, NF-κB, which leads to expression of pro-inflammatory genes.
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