Interaction between mineralocorticoid receptor and cAMP/CREB signaling.
Besides regulating water and electrolyte homeostasis, the mineralocorticoid receptor (MR) elicits pathophysiological effects in the renocardiovascular system. Although the MR's closest relative, the glucocorticoid receptor (GR), acts as a transcription factor at the same hormone-response-element (HRE), activated glucocorticoid receptor mediates very different effects. One explanation for this discrepancy is that the MR interacts with additional signaling pathways in the cytosol. In the literature, there are several indications for an interaction between aldosterone/MR and the cAMP/CREB signaling. Here we summarize the current knowledge of the cross-talk between the two signaling pathways, including some unpublished observations of our own that indicate that MR/CREB signaling is mediated by calcineurin and has potentially pathophysiological consequences.
Grossmann
Claudia
C
Julius-Bernstein-Institute of Physiology, Martin-Luther-University Halle-Wittenberg, Magdeburger Str. 6, 06097 Halle (Saale), Germany. claudia.grossmann@medizin.uni-halle.de
Ruhs
Stefanie
S
Seiferth
Anja
A
Gekle
Michael
M
D000818:Animals; D019703:Calcineurin / Q000378:metabolism; D000242:Cyclic AMP / Q000378:metabolism*; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism*; D006801:Humans; D018161:Receptors, Mineralocorticoid / Q000378:metabolism*; D015398:Signal Transduction
D017362:Cyclic AMP Response Element-Binding Protein; D018161:Receptors, Mineralocorticoid; D000242:Cyclic AMP; D019703:Calcineurin