Abstract
The “developmental origins of health and disease” theory indicates that many adult-onset diseases can originate in the earliest stages of life. The developing kidney has emerged as being particularly vulnerable to adverse in utero conditions leading to morphological and functional changes, namely renal programming. Emerging evidence indicates oxidative stress, an imbalance between reactive oxygen/nitrogen species (ROS/RNS) and antioxidant systems, plays a pathogenetic role in the developmental programming of kidney disease. Conversely, perinatal use of antioxidants has been implemented to reverse programming processes and prevent adult-onset diseases. We have termed this reprogramming. The focus of this review is twofold: (1) To summarize the current knowledge on oxidative stress implicated in renal programming and kidney disease of developmental origins; and (2) to provide an overview of reprogramming effects of perinatal antioxidant therapy on renal programming and how this may prevent adult-onset kidney disease. Although early-life oxidative stress is implicated in mediating renal programming and adverse offspring renal outcomes, and animal models provide promising results to allow perinatal antioxidants applied as potential reprogramming interventions, it is still awaiting clinical translation. This presents exciting new challenges and areas for future research.
Highlights
About 10% of the world’s population has chronic kidney disease (CKD) [1]
As we reviewed elsewhere [3], oxidative stress impacts renal programming in offspring born of dams exposed to diverse early-life insults, such as caloric restriction [29,30], lowprotein diet [31], maternal diabetes [32], preeclampsia [33,34], prenatal dexamethasone exposure [35], prenatal dexamethasone and postnatal high-fat diet [36], and maternal smoking [37]
Therapy in renal programming is evidenced by the protection against hypertension in adult offspring born of dams exposed to suramin [33], L-NAME [34], and dexamethasone combined with postnatal high-fat diet [36]
Summary
About 10% of the world’s population has chronic kidney disease (CKD) [1]. An estimated around 5–10 million people die per year from kidney disease globally [2]. Oxidative stress plays a significant role in developmental origins of kidney disease [11,12]. Emerging evidence indicates the imbalance between ROS and NO has been implicated in developmental origins of kidney disease [16,17,18]. The idea from DOHaD research opens up new avenues to reverse the programming process by early intervention aiming to prevent developmental origins of kidney disease in adulthood via so-called reprogramming [10]. Little is known on whether gestational supplementing with antioxidants can be protective on kidney disease programmed by a variety of early-life insults. The aim of this review is to give an overview of oxidative stress implicated in kidney disease of developmental origins.
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