Serum levels of ET-1, M30, and angiopoietins-1 and -2 in HELLP syndrome and preeclampsia compared to controls

Karakuş, Savaş; Akkar, Özlem Bozoklu; Yıldız, Çağlar; Sancakdar, Enver; Çetin, Meral; Çetin, Ali

doi:10.1007/s00404-015-3803-1

Cited by 31 publications

(22 citation statements)

References 53 publications

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“…In recent studies, this activation of the ET-1 system in preeclamptic or in HELLP syndrome pregnancies has been confirmed by different research groups [1 && , 3,4], and, most interestingly, this elevation of circulating ET-1 levels in preeclampsia has been shown to be closely related to the increased sFlt-1 levels in this syndrome [1 && ,3]. Activation of the endothelin system has repeatedly been reported in clinical preeclampsia, and also in different experimental preeclampsia models.…”

Section: Elevated Endothelin In Preeclampsiamentioning

confidence: 68%

Role of endothelin in preeclampsia and hypertension following antiangiogenesis treatment

Saleh

Danser

Meiracker

2016

Current Opinion in Nephrology and Hypertension

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Section: Elevated Endothelin In Preeclampsiamentioning

confidence: 68%

Role of endothelin in preeclampsia and hypertension following antiangiogenesis treatment

Saleh

Danser

Meiracker

2016

Current Opinion in Nephrology and Hypertension

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“…ET-1 levels are higher during later stages of PE and return to normal levels within 48 hours after delivery (Taylor et al, 1990), suggesting that ET-1 may be involved in the progression rather than the initiation of PE. However, in most studies serum ET-1 levels do not differ in PE versus Norm-Preg women, and higher levels of ET-1 are observed mainly in patients with HELLP syndrome (Naiker et al, 2001; Celik et al, 2013; Karakus et al, 2016). Of note, ET-1 is released in a paracrine fashion from EC directly on VSMCs, and the increases in ET-1 levels in PE may be localized in tissues.…”

Section: Increased Endothelium-derived Contracting Factors In Preementioning

confidence: 92%

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

Possomato-Vieira

Khalil

2016

Advances in Pharmacology

181

117

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Preeclampsia is a pregnancy-related disorder characterized by hypertension, and could lead to maternal and fetal morbidity and mortality. Although the causative factors and pathophysiological mechanisms are unclear, endothelial dysfunction is a major hallmark of preeclampsia. Clinical tests and experimental research have suggested that generalized endotheliosis in the systemic, renal, cerebral and hepatic circulation could decrease endothelium-derived vasodilators such as nitric oxide, prostacyclin and hyperpolarization factor and increase vasoconstrictors such as endothelin-1 and thromboxane A2, leading to increased vasoconstriction, hypertension and other manifestation of preeclampsia. In search for the upstream mechanisms that could cause endothelial dysfunction, certain genetic, demographic and environmental risk factors have been suggested to cause abnormal expression of uteroplacental integrins, cytokines and matrix metalloproteinases, leading to decreased maternal tolerance, apoptosis of invasive trophoblast cells, inadequate spiral arteries remodeling, reduced uterine perfusion pressure (RUPP), and placental ischemia/hypoxia. RUPP may cause imbalance between the anti-angiogenic factors soluble fms-like tyrosine kinase-1 and soluble endoglin and the pro-angiogenic factors vascular endothelial growth factor and placental growth factor, or stimulate the release of other circulating bioactive factors such as inflammatory cytokines, hypoxia-inducible factor-1, reactive oxygen species, and angiotensin AT1 receptor agonistic autoantibodies. These circulating factors could then target endothelial cells and cause generalized endothelial dysfunction. Therapeutic options are currently limited, but understanding the factors involved in endothelial dysfunction could help design new approaches for prediction and management of preeclampsia.

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“…In concordance with the findings of increased inflammation and altered cell composition, elevated serum levels of the caspase-cleaved cytokeratin 18 fragment M30 have been detected. M30 indicates an increased cellular apoptosis rate [148]. In addition, placental cytokine expression has been analyzed; however, contradicting results have been published.…”

Section: Immunological Backgroundmentioning

confidence: 98%

Immunology of hepatic diseases during pregnancy

2016

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The mother's immune system has to adapt to pregnancy accepting the semi-allograft fetus and preventing harmful effects to the developing child. Aberrations in feto-maternal immune adaptation may result in disease of the mother, such as liver injury. Five pregnancy-associated liver disorders have been described so far, however, little is known concerning immune alterations promoting the respective disease. These liver disorders are pre-eclampsia, hemolysis, elevated liver enzymes, low platelet count (HELLP), acute fatty liver, hyperemesis gravidarum, and intrahepatic cholestasis of pregnancy. On the other hand, pre-existing autoimmune liver injury of the mother can be affected by pregnancy. This review intends to summarize current knowledge linking feto-maternal immunology and liver inflammation with a special emphasis on novel potential biomarkers.

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Serum levels of ET-1, M30, and angiopoietins-1 and -2 in HELLP syndrome and preeclampsia compared to controls

Cited by 31 publications

References 53 publications

Role of endothelin in preeclampsia and hypertension following antiangiogenesis treatment

Role of endothelin in preeclampsia and hypertension following antiangiogenesis treatment

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

Immunology of hepatic diseases during pregnancy

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