[1]
Demir R, Kaufmann P, Castellucci M, Erbengi T, Kotowski A. Fetal vasculogenesis and angiogenesis in human placental villi. Acta Anat (Basel) 1989; 136: 190-203.
[2]
Red-Horse K, Zhou Y, Genbacev O, et al. Trophoblast differentiation during embryo implantation and formation of the maternal-fetal interface. J Clin Invest 2004; 114: 744-54.
[3]
Zhou Y, Damsky CH, Fisher SJ. Preeclampsia is associated with failure of human cytotrophoblasts to mimic a vascular adhesion phenotype. One cause of defective endovascular invasion in this syndrome? J Clin Invest 1997; 99: 2152-64.
[4]
Józkowicz A, Huk I, Nigisch A, et al. Heme oxygenase and angiogenic activity of endothelial cells: Stimulation by carbon monoxide and inhibition by tin protoporphyrin-IX. Antioxid Redox Signal 2003; 5: 155-62.
[5]
Maynard S, Epstein FH, Karumanchi SA. Preeclampsia and angiogenic imbalance. Annu Rev Med 2008; 59: 61-78.
[6]
Gilbert JS, Verzwyvelt J, Colson D, Arany M, Karumanchi SA, Granger JP. Recombinant vascular endothelial growth factor 121 infusion lowers blood pressure and improves renal function in rats with placental ischemia- induced hypertension. Hypertension 2010; 55: 380-5.
[7]
Warrington JP, George EM, Palei AC, Spradley FT, Granger JP. Recent advances in the understanding of the pathophysiology of preeclampsia. Hypertension 2013; 62: 666-73.
[8]
Zenclussen MJ, Linzke N, Schumacher A, et al. Heme oxygenase-1 is critically involved in placentation, spiral artery remodelling, and blood pressure regulation during murine pregnancy. Front Pharmacol 2015; 5: 291.
[9]
Wu L, Wang R. Carbon monoxide: Endogenous production, physiological functions and pharmacological applications. Pharmacol Rev 2005; 57: 585-630.
[10]
Cudmore M, Ahmad S, Al-Ani B, et al. Negative regulation of soluble Flt-1 and soluble endoglin release by heme oxygenase-1. Circulation 2007; 115: 1789-97.
[11]
Abraham NG, Kappas A. Pharmacological and clinical aspects of heme oxygenase. Pharmacol Rev 2008; 60: 79-127.
[12]
Kapur NK, Morine KJ, Letarte M. Endoglin: A critical mediator of cardiovascular health. Vasc Health Risk Manag 2013; 9: 195-206.
[13]
Kendall RL, Thomas KA. Inhibition of vascular endothelial cell growth factor activity by an endogenously encoded soluble receptor. PNAS 1993; 90: 10705-9.
[14]
Levine RL, Lam C, Qian C, et al. Soluble endoglin and other circulating antiangiogenic factors in preeclampsia. NEJM 2006; 355: 992-1005.
[15]
Padmini E, Lavanya D. HIF1α, TNFα and HO-1 modulation in placental explants during Preeclampsia. Int J Res Chem Environ 2014; 4: 85-92.
[16]
Barker DJ. Intrauterine programmes of coronary heart disease and stroke. Acta Paediatr 1997; 423: 178-82.
[17]
Haladay A. Early risk factors for cardiovascular disease. BNF Nutr Bull 1990; 15: 6-7.
[18]
Barker DJ, Osmond C, Golding J, Kuh D, Wadsworth ME. Growth in utero blood pressure in childhood and adult life and mortality from cardiovascular disease. BMJ 1989; 298: 564-7.
[19]
Barker DJP, Hunter PD. Osmonde, Margetts B, Simmonds SJ. Weight in infancy and death from ischaemic heart disease. Lancet 1989; 9: 577-80.
[20]
Zhao H, Wong RJ, Kalish FS, Nayak NR, Stevenson DK. Effect of heme oxygenase-1 deficiency on placental development. Placenta 2009; 30: 861-8.
[21]
Cudmore M, Ahmad S, Al-Ani B. Fujisaivaka t, Cuxall H, Chudasama K. Negative regulation of soluble Flt-1 and soluble endoglin release by heme oxygenase. Circulation 2007; 115: 1789-97.
[22]
St-Jacques S, Forte M, Lye SJ, Letarte M. Localization of endoglin, a transforming growth factor-beta binding protein, and of CD44 and integrins in placenta during the first trimester of pregnancy. Biol Reprod 1994; 51: 405-13.
[23]
Vitoratos N, Papakonstantinou K, Deliveliotou A, et al. Antepartum and postpartum serum heme oxygenase-1 levels in preeclamptic and normotensive pregnant women. In vivo 2011; 25: 445-50.
[24]
Romero R, Nien JK, Espinoza J, et al. A longitudinal study of angiogenic (placental growth factor) and anti-angiogenic (soluble endoglin and soluble VEGF receptor-1) factors in normal pregnancy and patients destined to develop preeclampsia and deliver a small-for-gestational-age neonate. J Matern Fetal Neonatal Med 2008; 21: 9-23.
[25]
Yinon Y, Nevo O, Xu J, et al. Severe intrauterine growth restriction pregnancies have increased placental endoglin levels: Hypoxic regulation via transforming growth factor-beta 3. Am J Pathol 2008; 172: 77-85.
[26]
Laskowska M, Laskowska K, Oleszczuk J. Endoglin in pregnancy complicated by fetal intrauterine growth restriction in normotensive and preeclamptic pregnant women: A comparison between preeclamptic patients with appropriate-for-gestational-age weight infants and healthy pregnant women. J Matern Fetal Neonatal Med 2012; 25: 806-11.
[27]
Zhou Y, McMaster M, Woo K, et al. Vascular endothelial growth factor ligands and receptors that regulate human cytotrophoblast survival are dysregulated in severe preeclampsia and hemolysis, elevated liver enzymes, and low platelets syndrome. Am J Pathol 2002; 160: 1405-23.
[28]
Nomenckova I, Serwadczak A, Oryo B, Jezkova K, Rathouskar J, Fikrova P. High soluble endoglin levels do not induce endothelial dysfunction in mouse aorta. PLoS One 2015; 10(3): e0119665.
[29]
Levine RJ, Thadhani R, Qian C, et al. Urinary placental growth factor and risk of preeclampsia. J Am Med Assoc 2005; 293: 77-85.
[30]
Buhimschi C, Baumbusch M, Dulay A, et al. The role of urinary soluble endoglin in the diagnosis of pre-eclampsia: Comparison with soluble fms-like tyrosine kinase 1 to placental growth factor ratio. BJOG 2010; 117: 321-30.
[31]
Cudmore MJ, Ahmad S, Sissaoui S, et al. Loss of Akt activity increases circulating soluble endoglin release in preeclampsia: Identification of inter-dependency between Akt-1 and heme oxygenase-1. Eur Heart J 2012; 33: 1150-8.
[32]
Mukar Y, Rikitake Y, Shiojima I, et al. Decreased vascular lesion formation in mice with inducible endothelial-specific expression of protein kinase Akt. J Clin Invest 2006; 116: 334-43.