Pre-eclampsia: excessive activation of a G protein-associated receptor?
Although the systemic physiological alterations present in pre-eclampsia appear disparate and unrelated, four of them (endothelial cell hyperplasia and alterations in uric acid, calcium, and prostaglandin homeostasis) are demonstrated here to mimic closely the pattern of intracellular alterations caused by the activation of a G protein-associated receptor. The implication of this is that the excessive activation of a particular G protein-associated receptor may play a central role in the pathogenesis of pre-eclampsia.
Coffey
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D001095:Arachidonic Acids / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D004730:Endothelium, Vascular / Q000473:pathology; D005234:Fatty Liver / Q000503:physiopathology; D005260:Female; D019204:GTP-Binding Proteins / Q000378:metabolism*; D006801:Humans; D006965:Hyperplasia; D008954:Models, Biological; D011225:Pre-Eclampsia / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000503:physiopathology; D011956:Receptors, Cell Surface / Q000378:metabolism*; D014527:Uric Acid / Q000097:blood
D001095:Arachidonic Acids; D011956:Receptors, Cell Surface; D014527:Uric Acid; D019204:GTP-Binding Proteins; D002118:Calcium