Inflammatory signaling mediators via nuclear receptors and transcription factors

Inflammatory signaling mediators via nuclear receptors and transcription factors encompass a broad class of proteins that regulate the genomic response to inflammatory stimuli. This group includes ligand-activated nuclear receptors, such as the glucocorticoid receptor (GR) and peroxisome proliferator-activated receptors (PPARs), as well as key transcription factors like NF-kappaB, AP-1, and STAT proteins (Glass & Ogawa, 2006, Nat Rev Immunol). These molecules function by binding to specific DNA sequences or interacting with other proteins to modulate the transcription of genes involved in the immune response, cell proliferation, and survival (Oeckinghaus & Ghosh, 2009, Cold Spring Harb Perspect Biol). Dysregulation of these pathways is a hallmark of chronic inflammatory conditions, including rheumatoid arthritis, asthma, and inflammatory bowel disease, as well as various malignancies (Libby, 2002, Nature). Pharmacological targeting of these mediators is a cornerstone of anti-inflammatory therapy, utilizing agonists like dexamethasone to activate anti-inflammatory pathways or inhibitors like JAK inhibitors to block pro-inflammatory signaling (Barnes, 2011, Br J Pharmacol). However, because these factors often have pleiotropic effects across multiple organ systems, therapeutic intervention can lead to significant safety concerns such as systemic immunosuppression and metabolic side effects (Ricote & Glass, 2007, Arterioscler Thromb Vasc Biol).

Other names

Nuclear receptor-mediated inflammatory signalingTranscription factor-driven inflammationInflammatory gene regulation pathwayGenomic inflammatory signaling

Modulation of gene transcription through the activation or inhibition of nuclear receptors (e.g., GR, PPARs) and transcription factors (e.g., NF-kappaB, STATs) that bind to specific DNA response elements to regulate the expression of pro-inflammatory and anti-inflammatory genes.