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Corticosteroid-sensitive pathways" refers to cellular and molecular cascades regulated by corticosteroids, primarily through the glucocorticoid and mineralocorticoid receptors. These receptors are intracellular ligand-activated transcription factors that, upon corticosteroid binding, translocate to the nucleus and modulate the expression of numerous genes involved in inflammation, metabolism, immunity, and cellular growth or death. The net effect of corticosteroid signaling is the suppression of inflammatory and immune responses, making these pathways central to the pharmacology of anti-inflammatory and immunosuppressive drugs. Given the broad gene regulatory activity and the range of physiological functions, these pathways are crucial therapeutic targets but are also associated with significant safety risks when perturbed by exogenous corticosteroids[1][3][6][8][9][10].
Ligand (corticosteroid) binding to the receptor facilitates nuclear translocation; Regulation of target gene expression via DNA binding (transactivation) or inhibition of other transcription factors (transrepression); Suppression of pro-inflammatory genes and promotion of anti-inflammatory genes[3][6][8]
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