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Loss of Akt activity increases circulating soluble endoglin release in preeclampsia: identification of inter-dependency between Akt-1 and heme oxygenase-1.

Melissa J MJ Cudmore, Shakil S Ahmad, Samir S Sissaoui, Wenda W Ramma, Bin B Ma, Takeshi T Fujisawa, Bahjat B Al-Ani, Keqing K Wang, Meng M Cai, Fatima F Crispi, Peter W PW Hewett, Eduard E Gratacós, Stuart S Egginton, and Asif A Ahmed

Eur Heart J 33(9):1150-8 (2012) PMID 21411816 PMCID PMC3341632

Endothelial dysfunction is a hallmark of preeclampsia. Desensitization of the phosphoinositide 3-kinase (PI3K)/Akt pathway underlies endothelial dysfunction and haeme oxygenase-1 (HO-1) is decreased in preeclampsia. To identify therapeutic targets, we sought to assess whether these two regulators act to suppress soluble endoglin (sEng), an antagonist of transforming growth factor-β (TGF-β) signalling, which is known to be elevated in preeclampsia.

DOI: 10.1093/eurheartj/ehr065
Version: za2963e q8zae q8zb3 q8zc9 q8zd3 q8zee q8zf0 q8zg8

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