首页> 美国卫生研究院文献>International Journal of Molecular Sciences >Targeting on Asymmetric Dimethylarginine-Related Nitric Oxide-Reactive Oxygen Species Imbalance to Reprogram the Development of Hypertension
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Targeting on Asymmetric Dimethylarginine-Related Nitric Oxide-Reactive Oxygen Species Imbalance to Reprogram the Development of Hypertension

机译:针对不对称的二甲基精氨酸相关的一氧化氮反应性氧气物种失衡以重新编程高血压的发展

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摘要

Adult-onset diseases, including hypertension, can originate from early life, known as the developmental origins of health and disease (DOHaD). Because the developing kidney is vulnerable to early-life insults, renal programming is considered key in the developmental programming of hypertension. Asymmetric dimethylarginine (ADMA), an endogenous nitric oxide (NO) synthase inhibitor, can regulate the NO–reactive oxygen species (ROS) balance, and is involved in the development of hypertension. Reprogramming interventions aimed at NO-ROS balance can be protective in both genetic and developmentally programmed hypertension. Here we review several emergent themes of the DOHaD approach regarding the impact of ADMA-related NO-ROS imbalance on programmed hypertension. We focus on the kidney in the following areas: mechanistic insights to interpret programmed hypertension; the impact of ADMA-related NO-ROS imbalance in both genetic and acquired animal models of hypertension; alterations of the renal transcriptome in response to ADMA in the developing kidney; and reprogramming strategies targeting ADMA-related NO-ROS balance to prevent programmed hypertension.
机译:成人发作的疾病(包括高血压)可以起源于早期生活,被称为健康与疾病的发展起源(DOHaD)。由于发育中的肾脏容易受到早期生命的伤害,因此肾脏编程被认为是高血压发展编程中的关键。不对称二甲基精氨酸(ADMA)是一种内源性一氧化氮(NO)合酶抑制剂,可以调节NO-活性氧(ROS)的平衡,并参与高血压的发展。针对NO-ROS平衡的重编程干预措施可以在遗传性和发育性高血压中起到保护作用。在这里,我们回顾了DOHaD方法的几个新兴主题,这些主题涉及ADMA相关的NO-ROS不平衡对程序性高血压的影响。我们主要关注以下领域的肾脏:解释程序性高血压的机制见解;与ADMA相关的NO-ROS失衡对遗传和获得性高血压动物模型的影响;在发育中的肾脏中,响应ADMA的肾脏转录组的改变;针对ADMA相关的NO-ROS平衡的重编程策略,以预防程序性高血压。

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