Maternal melatonin or N-acetylcysteine therapy regulates hydrogen sulfide-generating pathway and renal transcriptome to prevent prenatal NG-Nitro-L-arginine-methyl ester (L-NAME)-induced fetal programming of hypertension in adult male offspring

Tain, You‐Lin; Lee, Chien-Te; Chan, Julie Y.H.; Hsu, Chien‐Ning

doi:10.1016/j.ajog.2016.07.036

Cited by 61 publications

(129 citation statements)

References 28 publications

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“…It is highly vulnerable to oxidant injury. A number of animal models suggest oxidative stress involved in renal programming, including caloric restriction [40], maternal diabetes [41], prenatal dexamethasone exposure [43], high fructose intake [50], prenatal dexamethasone and postnatal high-fat diet [51], preeclampsia [52,53], maternal smoking [54], and low-protein diet [55]. Additionally, emerging evidence supports that NO-ROS imbalance is important for programmed hypertension [15,56].…”

Section: Mechanisms Of Renal Programmingmentioning

confidence: 99%

“…Glutathione (GSH) is the major intracellular antioxidant [112]. Our previous study demonstrated that N -acetylcysteine can increase GSH and reduce oxidative stress to prevent the development of hypertension in different models of renal programming [51,52,53]. Additional studies are required to unravel the impacts of the glutathione pathway on oxidative stress and programmed kidney disease.…”

Section: Changes In Renal Transcriptome In Response To Early-life mentioning

confidence: 99%

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Developmental Origins of Chronic Kidney Disease: Should We Focus on Early Life?

Tain

Hsu

2017

IJMS

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103

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Chronic kidney disease (CKD) is becoming a global burden, despite recent advances in management. CKD can begin in early life by so-called “developmental programming” or “developmental origins of health and disease” (DOHaD). Early-life insults cause structural and functional changes in the developing kidney, which is called renal programming. Epidemiological and experimental evidence supports the proposition that early-life adverse events lead to renal programming and make subjects vulnerable to developing CKD and its comorbidities in later life. In addition to low nephron endowment, several mechanisms have been proposed for renal programming. The DOHaD concept opens a new window to offset the programming process in early life to prevent the development of adult kidney disease, namely reprogramming. Here, we review the key themes on the developmental origins of CKD. We have particularly focused on the following areas: evidence from human studies support fetal programming of kidney disease; insight from animal models of renal programming; hypothetical mechanisms of renal programming; alterations of renal transcriptome in response to early-life insults; and the application of reprogramming interventions to prevent the programming of kidney disease.

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Section: Mechanisms Of Renal Programmingmentioning

confidence: 99%

Section: Changes In Renal Transcriptome In Response To Early-life mentioning

confidence: 99%

Developmental Origins of Chronic Kidney Disease: Should We Focus on Early Life?

Tain

Hsu

2017

IJMS

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103

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“…Last, in melatonin-deficient hypertension model, the RAS is activated [41]. In contrast, melatonin treatment can regulate RAS components and prevent the elevation of BP in several programming models of hypertension [35,40,42,43]. All of these observations provide a close link between melatonin and other mechanisms involved in developmental programming (Figure 1).…”

Section: Mechanisms Of Developmental Programmingmentioning

confidence: 99%

“…As shown in Table 1, a variety of early-life insults have been reported to cause developmental programming of adult diseases. These environmental and nutritional insults include maternal undernutrition [42], N G -nitro- l -arginine-methyester (L-NAME) induced preeclampsia [43], high-fructose consumption [63], prenatal hypoxia [64], glucocorticoid exposure [33,36,37,38,39,40,65], high-fat diet [40], and constant light exposure [66]. These insults induce a number of programming effects on adult offspring including hypertension, reduced nephron number, cognition deficit, behavior dysfunction, obesity, and liver steatosis.…”

Section: Melatonin As a Reprogramming Therapy In Animal Models Of mentioning

confidence: 99%

“…Thus, the influence of melatonin on adult offspring should be considered as reprogramming instead of direct effects. So far, a few mechanisms, including oxidative stress [42,43,63,65], epigenetic regulation [38,39,40], reduction in nephron numbers [39], and alterations of the RAS [40] have been linked to the reprogramming effects of melatonin.…”

Section: Melatonin As a Reprogramming Therapy In Animal Models Of mentioning

confidence: 99%

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Developmental Programming of Adult Disease: Reprogramming by Melatonin?

Tain

Huang

Hsu

2017

IJMS

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Adult-onset chronic non-communicable diseases (NCDs) can originate from early life through so-called the “developmental origins of health and disease” (DOHaD) or “developmental programming”. The DOHaD concept offers the “reprogramming” strategy to shift the treatment from adulthood to early life, before clinical disease is apparent. Melatonin, an endogenous indoleamine produced by the pineal gland, has pleiotropic bioactivities those are beneficial in a variety of human diseases. Emerging evidence support that melatonin is closely inter-related to other proposed mechanisms contributing to the developmental programming of a variety of chronic NCDs. Recent animal studies have begun to unravel the multifunctional roles of melatonin in many experimental models of developmental programming. Even though some progress has been made in research on melatonin as a reprogramming strategy to prevent DOHaD-related NCDs, future human studies should aim at filling the translational gap between animal models and clinical trials. Here, we review several key themes on the reprogramming effects of melatonin in DOHaD research. We have particularly focused on the following areas: mechanisms of developmental programming; the interrelationship between melatonin and mechanisms underlying developmental programming; pathophysiological roles of melatonin in pregnancy and fetal development; and insight provided by animal models to support melatonin as a reprogramming therapy. Rates of NCDs are increasing faster than anticipated all over the world. Hence, there is an urgent need to understand reprogramming mechanisms of melatonin and to translate experimental research into clinical practice for halting a growing list of DOHaD-related NCDs.

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Primary Pediatric Hypertension: Current Understanding and Emerging Concepts

et al. 2017

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The rising prevalence of primary pediatric hypertension and its tracking into adult hypertension point to the importance of determining its pathogenesis to gain insights into its current and emerging management. Considering that the intricate control of BP is governed by a myriad of anatomical, molecular biological, biochemical, and physiological systems, multiple genes are likely to influence an individual's BP and susceptibility to develop hypertension. The long-term regulation of BP rests on renal and non-renal mechanisms. One renal mechanism relates to sodium transport. The impaired renal sodium handling in primary hypertension and salt sensitivity may be caused by aberrant counter-regulatory natriuretic and anti-natriuretic pathways. The sympathetic nervous and renin-angiotensin-aldosterone systems are examples of antinatriuretic pathways. An important counter-regulatory natriuretic pathway is afforded by the renal autocrine/paracrine dopamine system, aberrations of which are involved in the pathogenesis of hypertension, including that associated with obesity. We present updates on the complex interactions of these two systems with dietary salt intake in relation to obesity, insulin resistance, inflammation, and oxidative stress. We review how insults during pregnancy such as maternal and paternal malnutrition, glucocorticoid exposure, infection, placental insufficiency, and treatments during the neonatal period have long-lasting effects in the regulation of renal function and BP. Moreover, these effects have sex differences. There is a need for early diagnosis, frequent monitoring, and timely management due to increasing evidence of premature target organ damage. Large controlled studies are needed to evaluate the long-term consequences of the treatment of elevated BP during childhood, especially to establish the validity of the current definition and treatment of pediatric hypertension.

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Maternal melatonin or N-acetylcysteine therapy regulates hydrogen sulfide-generating pathway and renal transcriptome to prevent prenatal NG-Nitro-L-arginine-methyl ester (L-NAME)-induced fetal programming of hypertension in adult male offspring

Cited by 61 publications

References 28 publications

Developmental Origins of Chronic Kidney Disease: Should We Focus on Early Life?

Developmental Origins of Chronic Kidney Disease: Should We Focus on Early Life?

Developmental Programming of Adult Disease: Reprogramming by Melatonin?

Primary Pediatric Hypertension: Current Understanding and Emerging Concepts

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