Roles of Nitric Oxide and Asymmetric Dimethylarginine in Pregnancy and Fetal Programming

Huang, Laura; Hsieh, Chih-Sung; Chang, Kow-Aung; Tain, You‐Lin

doi:10.3390/ijms131114606

Cited by 62 publications

(55 citation statements)

References 101 publications

(127 reference statements)

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“…These conditions can cause increased oxidative stress either in the mother or the fetus, which may result in the programming of diseases in the offspring at a later stage [58,66]. …”

Section: Redox and Epigenetic Mechanisms In Fetal Programmingmentioning

confidence: 99%

“…Maternal adversities leading to dysregulation of placental development originated from preimplantation affecting the course of pregnancy were shown in both animal and human studies to alter the epigenetic process (e.g., DNA methylation, histone modifications, and genome imprinting) and result in preeclampsia and dismal fetal outcomes [66,69]. A recent study showed altered global DNA methylation patterns in preeclampsia placentas and its association with blood pressure [129].…”

Section: The Roles Of Melatonin In Compromised Pregnanciesmentioning

confidence: 99%

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Roles of Melatonin in Fetal Programming in Compromised Pregnancies

Chen

Sheen

Tiao

et al. 2013

IJMS

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Compromised pregnancies such as those associated with gestational diabetes mellitus, intrauterine growth retardation, preeclampsia, maternal undernutrition, and maternal stress may negatively affect fetal development. Such pregnancies may induce oxidative stress to the fetus and alter fetal development through the epigenetic process that may affect development at a later stage. Melatonin is an oxidant scavenger that reverses oxidative stress during the prenatal period. Moreover, the role of melatonin in epigenetic modifications in the field of developmental programming has been studied extensively. Here, we describe the physiological function of melatonin in pregnancy and discuss the roles of melatonin in fetal programming in compromised pregnancies, focusing on its involvement in redox and epigenetic mechanisms.

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“…These conditions can cause increased oxidative stress either in the mother or the fetus, which may result in the programming of diseases in the offspring at a later stage [58,66]. …”

Section: Redox and Epigenetic Mechanisms In Fetal Programmingmentioning

confidence: 99%

Section: The Roles Of Melatonin In Compromised Pregnanciesmentioning

confidence: 99%

Roles of Melatonin in Fetal Programming in Compromised Pregnancies

Chen

Sheen

Tiao

et al. 2013

IJMS

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“…Among the guanidine compounds listed as uremic toxins [2], ADMA and SDMA and have been increasingly recognized as putative toxic non-proteinogenic amino acids in a wide range of human diseases over the past decades [3,4,5,6,7,8,9,10,11]. …”

Section: Introductionmentioning

confidence: 99%

“…Given that NO has pleiotropic bioactivities, it is not surprising that a variety of important biological functions are regulated by ADMA and SDMA. Emerging clinical and experimental evidence indicates that ADMA and SDMA are involved in the pathophysiology of endothelial dysfunction [13], atherosclerosis [4], oxidative stress [14,15], inflammation [16,17], uremia [8], apoptosis, [18], autophagy [19], and impaired immunological function [20]. …”

Section: Introductionmentioning

confidence: 99%

Toxic Dimethylarginines: Asymmetric Dimethylarginine (ADMA) and Symmetric Dimethylarginine (SDMA)

Tain

Hsu

2017

Toxins

202

195

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Asymmetric and symmetric dimethylarginine (ADMA and SDMA, respectively) are toxic, non-proteinogenic amino acids formed by post-translational modification and are uremic toxins that inhibit nitric oxide (NO) production and play multifunctional roles in many human diseases. Both ADMA and SDMA have emerged as strong predictors of cardiovascular events and death in a range of illnesses. Major progress has been made in research on ADMA-lowering therapies in animal studies; however, further studies are required to fill the translational gap between animal models and clinical trials in order to treat human diseases related to elevated ADMA/SDMA levels. Here, we review the reported impacts of ADMA and SDMA on human health and disease, focusing on the synthesis and metabolism of ADMA and SDMA; the pathophysiological roles of these dimethylarginines; clinical conditions and animal models associated with elevated ADMA and SDMA levels; and potential therapies against ADMA and SDMA. There is currently no specific pharmacological therapy for lowering the levels and counteracting the deleterious effects of ADMA and SDMA. A better understanding of the mechanisms underlying the impact of ADMA and SDMA on a wide range of human diseases is essential to the development of specific therapies against diseases related to ADMA and SDMA.

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“…Maternal plasma NO regulates feto-placental vascular activity and placental flow [3]. The activity of constitutive NO synthase is dependent on ADMA.…”

Section: Discussionmentioning

confidence: 99%