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Intensive Care Medicine Experimental
Fig. 1 | Intensive Care Medicine Experimental

Fig. 1

From: Impact of downstream effects of glucocorticoid receptor dysfunction on organ function in critical illness-associated systemic inflammation

Fig. 1

After the activation of the hypothalamus by external triggers, corticotropin-releasing factor (CRF) acts on the anterior pituitary to release proopiomelanocortin (POMC), which in turn is a proteolytic cleaved in adrenocorticotropic hormone (ACTH) and activates the production of enzymes for the corticosteroid synthesis in the adrenal glands. Glucocorticoids act in a negative feedback mechanism to regulate their own production. In humans, cortisone is converted by 11-β-hydroxysteroid-dehydrogenase-1 (11β-HSD1) to cortisol and vice versa by 11β-HSD2. In rodents, the 11-dehydrocorticosterone is converted to corticosterone and vice versa

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