Inflammatory Gene Suppression is the clinical goal of reducing the transcriptional activity of genes responsible for encoding pro-inflammatory cytokines, chemokines, and acute-phase proteins. This suppression aims to mitigate chronic, low-grade systemic inflammation, which is a major driver of age-related diseases and endocrine dysfunction, including insulin resistance. It represents a molecular-level strategy for managing inflammatory burden.
Origin
This term is rooted in molecular immunology and nutritional genomics, where the focus is on modulating gene expression through dietary and lifestyle factors, a concept known as nutrigenomics. The identification of transcription factors like NF-κB as central regulators of inflammatory genes provided the molecular target for this suppression.
Mechanism
Suppression is primarily achieved by activating nuclear receptors and transcription factors that counteract the effects of NF-κB, often through specific nutritional compounds or hormonal modulation. For example, certain fatty acids or hormonal metabolites can bind to receptors like PPARs, which then interfere with the inflammatory cascade. Reducing the chronic activation of these genes lowers the circulating levels of inflammatory markers, thereby improving tissue sensitivity to key hormones.
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