Genomic and nongenomic effects of steroids

The effects of glucocorticoids are mediated by cytosolic glucocorticoid receptors and result from both genomic and nongenomic mechanisms that also have a role in the therapeutic effects of these agents [ 1-3 ]. The AEs appear to result largely from transactivation that leads to increased expression of regulatory and antiinflammatory proteins [ 2 ]; by contrast, many of the clinically desirable effects appear to result primarily from transrepression, which results in the decreased production of proinflammatory proteins. Nongenomic effects of glucocorticoids include rapid, nonspecific interactions of glucocorticoids with cellular membranes, nongenomic effects medicated by cytosolic glucocorticoid receptors, and specific interactions with membrane-bound glucocorticoid receptors [ 2 ].

Genomic and nongenomic effects of steroids

genomic and nongenomic effects of steroids

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