Endothelin-1 receptor antagonists in fetal development and pulmonary arterial hypertension

Raaf, Michiel Alexander de; Beekhuijzen, Manon; Guignabert, Christophe; Vonk‐Noordegraaf, Anton; Bogaard, Harm Jan

doi:10.1016/j.reprotox.2015.06.048

Cited by 31 publications

(15 citation statements)

References 92 publications

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“…Determination of serum tryptophan and serotonin concentration can indirectly reflect the body's vasoconstriction. Research suggests ET-1-ROCK interactions have already been proven to contribute to decreased alveolar and vascular growth and pulmonary hypertension (PH) in experimental bronchopulmonary dysplasia 19,36 confirmed that ET-1-mediated positive inotropic effects and myocardial fetal gene induction further lead to PH. Interestingly, recent reports from Josefa et al demonstrated that melatonin, which is an indoleamine that is synthesized from tryptophan under the control of the enzymes aryl alkylamine N-acetyltransferase (AANAT) and acetyl serotonin methyltransferase (ASMT), can reduce endothelin-1 expression through the inactivation of FoxO-1 and NF-κβ, playing an important role in colon cancer 37 .…”

Section: Discussionmentioning

confidence: 99%

EDN1 gene potentially involved in the development of acute mountain sickness

Liu

Zhang

et al. 2020

Sci Rep

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Previous investigations have indicated that environmental and genetic factors collectively contribute to the development of acute mountain sickness (AMS), but whether the EDN1 gene is involved in AMS remains to be elucidated. A total of 356 healthy male soldiers who had not traveled to high altitudes in the previous 12 months were enrolled in our study. All participants were taken by plane from 500 m (Chengdu in Sichuan Province) to a 3700 m highland (Lhasa) within 2 hours. Clinical data were collected within 24 hours, and pulmonary function parameters were completed simultaneously. Genotypes were obtained by using iMLDR genotyping assays. A total of 237 soldiers (66.57%) presented AMS symptoms, including headache, dizziness, gastrointestinal upset and fatigue. Soldiers with AMS showed an increase in heart rate (HR), plasma tryptophan and serotonin, and a decrease in SaO2, FEV1, PEF, FVC, V75, V50, V25 and MMF (all P < 0.01). Notably, allele T in single nucleotide polymorphism (SNP) rs2070699 showed a positive correlation with the occurrence of AMS. A general linear regression analysis showed that rs2060799, Mean Arterial Pressure (MAP), SaO2, FVC, tryptophan and serotonin were independent predictors for the occurrence of AMS. Importantly, the area under the curve (AUC) values for tryptophan (0.998), serotonin (0.912) and FVC (0.86) had diagnostic specificity and sensitivity. Our results demonstrated that AMS is accompanied by changes in lung function parameters, increased plasma tryptophan and serotonin levels, and that the EDN1 polymorphism is a potential risk factor for AMS.

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Section: Discussionmentioning

confidence: 99%

EDN1 gene potentially involved in the development of acute mountain sickness

Liu

Zhang

et al. 2020

Sci Rep

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“…It is also used to reduce the number of digital ulcers in people with systemic scleroderma (Abraham & Steen, ). This drug causes harm in cardiopulmonary fetal development and renders hormonal contraceptives ineffective (de Raaf, Beekhuijzen, Guignabert, Vonk Noordegraaf, & Bogaard, ).…”

Section: Chemical Agentsmentioning

confidence: 99%

“…Additionally, administration of endothelin receptor blockers (i.e., bosentan) to treat it during the fetal period decreased pulmonary vascular resistance levels and precluded a correct right ventricle development. Finally, Endothelin receptor antagonists were shown to have negative inotropic effects on right ventricle contractility (de Raaf et al, ).…”

Section: Chemical Agentsmentioning

confidence: 99%

The role of teratogens in neural crest development

Cerrizuela

Vega-Lopez

Aybar

2020

Birth Defects Research

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The neural crest (NC), discovered by Wilhelm His 150 years ago, gives rise to a multipotent migratory embryonic cell population that generates a remarkably diverse and important array of cell types during the development of the vertebrate embryo. These cells originate in the neural plate border (NPB), which is the ectoderm between the neural plate and the epidermis. They give rise to the neurons and glia of the peripheral nervous system, melanocytes, chondrocytes, smooth muscle cells, odontoblasts and neuroendocrine cells, among others. Neurocristopathies are a class of congenital diseases resulting from the abnormal induction, specification, migration, differentiation or death of NC cells (NCCs) during embryonic development and have an important medical and societal impact. In general, congenital defects affect an appreciable percentage of newborns worldwide. Some of these defects are caused by teratogens, which are agents that negatively impact the formation of tissues and organs during development. In this review, we will discuss the teratogens linked to the development of many birth defects, with a strong focus on those that specifically affect the development of the NC, thereby producing neurocristopathies.Although increasing attention is being paid to the effect of teratogens on embryonic development in general, there is a strong need to critically evaluate the specific role of these agents in NC development. Therefore, increased understanding of the role of these factors in NC development will contribute to the planning of strategies aimed at the prevention and treatment of human neurocristopathies, whose etiology was previously not considered.

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“…This drug safety program is required by the FDA to reduce the risk of fetal harm of certain medications. 50 As part of this program, women of childbearing potential must have a negative pregnancy test prior to the initiation of therapy, monthly during treatment and within 1 month of stopping it. In addition, given the potential for hepatotoxicity, bosentan requires monthly serum transaminase and bilirubin determinations.…”

Section: Factors Affecting Medication Adherencementioning

confidence: 99%

Treatment Discontinuation or Interruption in Pulmonary Arterial Hypertension

Narechania

Torbic

Tonelli

2019

J Cardiovasc Pharmacol Ther

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Pulmonary arterial hypertension (PAH) is a progressive disease, which can be potentially fatal. The management of a complex disease like PAH requires a multidisciplinary approach from a team consisting of physicians, nurses, social workers, and pharmacists. Adherence to PAH-specific therapy is one of the key factors in the management of this disease. Poor adherence to treatment is a common problem in PAH as it is in many chronic diseases. Management of medication interruptions is a challenge in patients with PAH that can lead to negative consequences. However, for most PAH-specific drugs, there are no clear guidelines on how to manage temporary or abrupt medication discontinuations. In this review, we summarized the available literature and provide suggestions on how to manage interruptions of PAH-specific therapies.

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Endothelin-1 receptor antagonists in fetal development and pulmonary arterial hypertension

Cited by 31 publications

References 92 publications

EDN1 gene potentially involved in the development of acute mountain sickness

EDN1 gene potentially involved in the development of acute mountain sickness

The role of teratogens in neural crest development

Treatment Discontinuation or Interruption in Pulmonary Arterial Hypertension

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