The role of the renin–angiotensin–aldosterone system in preeclampsia: genetic polymorphisms and microRNA
- 1Department of Pathophysiology, School of Basic Medical Sciences, Capital Medical University, 10 Xitoutiao, You An Men, Beijing 100069, People's Republic
of China
2Department of Physiology, Shanxi Medical University, Taiyuan, Shanxi 030001, People's Republic of China
- Correspondence should be addressed to H Liu; Email: liuhr2000{at}126.com
-
Figure 1
Despite a significant decrease in most components, elevated sensitivity of AT1R and its increased amount seem to account for hypertension and intrauterine growth retardation in preeclampsia. The red arrows indicate an increase in concentration while the blue arrows indicate a decrease in concentration.
-
Figure 2
Adrenocortical steroidogenic pathway for ALD biosynthesis. StAR is paramount for the rate-limiting step of movement of cholesterol into the mitochondria, where cholesterol is cleaved by CYP11A1 to pregnenolone. Then the compound is catalyzed by HSD3B2, CYP21A2, and CYP11B2 into ALD. Urinary steroid metabolites can be quantified to assess the enzyme activities of CYP11B2 consisting of three different enzymatic reactions. In preeclampsia, the decreased TH-Aldo level accompanied by elevated 18-OH-THA indicates impaired CYP11B2 activity, specifically 18-oxidase activity. DOC, 11-deoxycorticosterone; THDOC, tetrahydro-11-deoxycorticosterone; THB, tetrahydrocorticosterone; THA, tetrahydro-11-dehydrocorticosterone; 18-OH-THA, 18-OH-tetrahydrocorticosterone; TH-Aldo, tetrahydroaldosterone. The red arrows indicate an increase in concentration while the blue arrows indicate a decrease in concentration.
- © 2013 Society for Endocrinology
