Auto-antibodies against the angiotensin II type I receptor in women with uteroplacental acute atherosis and preeclampsia at delivery and several years postpartum

Rieber-Mohn, Amalie Bjerke; Sugulle, Meryam; Wallukat, Gerd; Alnæs-Katjavivi, Patji; Størvold, Gunnar; Bolstad, Nils; Redman, Christopher W.G.; Dechend, Ralf; Staff, Anne Cathrine

doi:10.1016/j.jri.2018.05.008

Cited by 23 publications

(24 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, previous studies have shown that maternal AT1-AA persisted up to 27 months after pregnancy in 17.2% of women with preeclampsia compared to 2.9% in women with normotensive pregnancy [ 49 ]. Recently, a follow up study on circulating AT1-AA levels at five to eight years postpartum was published which showed that AT1-AA was persistently found in women with a history of preeclampsia, which might relate to their future CVD risk [ 50 ].…”

Section: Molecular Factors Resulting From Inadequate Uteroplacental Perfusion Leading To Preeclampsiamentioning

confidence: 99%

Defective Uteroplacental Vascular Remodeling in Preeclampsia: Key Molecular Factors Leading to Long Term Cardiovascular Disease

Hong

Kim

Hyun

et al. 2021

IJMS

View full text Add to dashboard Cite

Preeclampsia is a complex hypertensive disorder in pregnancy which can be lethal and is responsible for more than 70,000 maternal deaths worldwide every year. Besides the higher risk of unfavorable obstetric outcomes in women with preeclampsia, another crucial aspect that needs to be considered is the association between preeclampsia and the postpartum cardiovascular health of the mother. Currently, preeclampsia is classified as one of the major risk factors of cardiovascular disease (CVD) in women, which doubles the risk of venous thromboembolic events, stroke, and ischemic heart disease. In order to comprehend the pathophysiology behind the linkage between preeclampsia and the development of postpartum CVD, a thorough understanding of the abnormal uteroplacental vascular remodeling in preeclampsia is essential. Therefore, this review aims to summarize the current knowledge of the defective process of spiral artery remodeling in preeclampsia and how the resulting placental damage leads to excessive angiogenic imbalance and systemic inflammation in long term CVD. Key molecular factors in the pathway—including novel findings of microRNAs—will be discussed with suggestions of future management strategies of preventing CVD in women with a history of preeclampsia.

show abstract

Section: Molecular Factors Resulting From Inadequate Uteroplacental Perfusion Leading To Preeclampsiamentioning

confidence: 99%

Defective Uteroplacental Vascular Remodeling in Preeclampsia: Key Molecular Factors Leading to Long Term Cardiovascular Disease

Hong

Kim

Hyun

et al. 2021

IJMS

View full text Add to dashboard Cite

show abstract

“…We have postulated a role in acute atherosis for activating antibodies against the angiotensin II type 1 receptor (AA-AT 1 ), after demonstrating a clear association between AA-AT 1 and preeclampsia ( 54 – 56 ). Based on our cesarean delivery population, we were unable to demonstrate any association between AA-AT 1 and acute atherosis ( 21 ). However, angiotensin II is known to work synergistically with ET-1 ( 57 ), and studying both of these vasoconstrictor systems simultaneously would shed more light on the possible involvement of G-protein cascades in acute atherosis development.…”

Section: Acute Atherosis Etiologymentioning

confidence: 89%

Acute Atherosis Lesions at the Fetal-Maternal Border: Current Knowledge and Implications for Maternal Cardiovascular Health

et al. 2021

Self Cite

View full text Add to dashboard Cite

Decidua basalis, the endometrium of pregnancy, is an important interface between maternal and fetal tissues, made up of both maternal and fetal cells. Acute atherosis is a uteroplacental spiral artery lesion. These patchy arterial wall lesions containing foam cells are predominantly found in the decidua basalis, at the tips of the maternal arteries, where they feed into the placental intervillous space. Acute atherosis is prevalent in preeclampsia and other obstetric syndromes such as fetal growth restriction. Causal factors and effects of acute atherosis remain uncertain. This is in part because decidua basalis is challenging to sample systematically and in large amounts following delivery. We summarize our decidua basalis vacuum suction method, which facilitates tissue-based studies of acute atherosis. We also describe our evidence-based research definition of acute atherosis. Here, we comprehensively review the existing literature on acute atherosis, its underlying mechanisms and possible short- and long-term effects. We propose that multiple pathways leading to decidual vascular inflammation may promote acute atherosis formation, with or without poor spiral artery remodeling and/or preeclampsia. These include maternal alloreactivity, ischemia-reperfusion injury, preexisting systemic inflammation, and microbial infection. The concept of acute atherosis as an inflammatory lesion is not novel. The lesions themselves have an inflammatory phenotype and resemble other arterial lesions of more extensively studied etiology. We discuss findings of concurrently dysregulated proteins involved in immune regulation and cardiovascular function in women with acute atherosis. We also propose a novel hypothesis linking cellular fetal microchimerism, which is prevalent in women with preeclampsia, with acute atherosis in pregnancy and future cardiovascular and neurovascular disease. Finally, women with a history of preeclampsia have an increased risk of premature cardiovascular disease. We review whether presence of acute atherosis may identify women at especially high risk for premature cardiovascular disease.

show abstract

“…A number of studies have now indicated that women with PE produce this novel agonistic autoantibody to the AT1-AA during pregnancy and up to 8 years after delivery. 65,66 One animal model used to examine the role of AT1AA is the AT1-AA chronic excess model where purified AT1-AA is infused into normal pregnant rats. A number of investigators have shown that AT1-AA signaling, via the AT1 receptor, results in a variety of physiological effects, including TNF-a and ROS generation, both of which have been implicated in PE.…”

Section: Models Used To Examine Role Of Agnostic Angiotensin II Type ...mentioning

confidence: 99%

Animal models of preeclampsia: investigating pathophysiology and therapeutic targets

Bakrania

George

Granger

2022

American Journal of Obstetrics and Gynecology

View full text Add to dashboard Cite

Auto-antibodies against the angiotensin II type I receptor in women with uteroplacental acute atherosis and preeclampsia at delivery and several years postpartum

Cited by 23 publications

References 31 publications

Defective Uteroplacental Vascular Remodeling in Preeclampsia: Key Molecular Factors Leading to Long Term Cardiovascular Disease

Defective Uteroplacental Vascular Remodeling in Preeclampsia: Key Molecular Factors Leading to Long Term Cardiovascular Disease

Acute Atherosis Lesions at the Fetal-Maternal Border: Current Knowledge and Implications for Maternal Cardiovascular Health

Animal models of preeclampsia: investigating pathophysiology and therapeutic targets

Contact Info

Product

Resources

About