Tain You-Lin, Hsu Chien-Ning
Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan.
College of Medicine, Chang Gung University, Taoyuan 333, Taiwan.
Antioxidants (Basel). 2022 Oct 26;11(11):2108. doi: 10.3390/antiox11112108.
Metabolic syndrome (MetS) is a worldwide public health issue characterized by a set of risk factors for cardiovascular disease. MetS can originate in early life by developmental programming. Increasing evidence suggests that oxidative stress, which is characterized as an imbalance between reactive oxygen species (ROS), nitric oxide (NO), and antioxidant systems, plays a decisive role in MetS programming. Results from human and animal studies indicate that maternal-derived insults induce MetS later in life, accompanied by oxidative stress programming of various organ systems. On the contrary, perinatal use of antioxidants can offset oxidative stress and thereby prevent MetS traits in adult offspring. This review provides an overview of current knowledge about the core mechanisms behind MetS programming, with particular focus on the occurrence of oxidative-stress-related pathogenesis as well as the use of potential oxidative-stress-targeted interventions as a reprogramming strategy to avert MetS of developmental origins. Future clinical studies should provide important proof of concept for the effectiveness of these reprogramming interventions to prevent a MetS epidemic.
代谢综合征(MetS)是一个全球性的公共卫生问题,其特征是一系列心血管疾病风险因素。MetS可通过发育编程在生命早期产生。越来越多的证据表明,以活性氧(ROS)、一氧化氮(NO)和抗氧化系统之间失衡为特征的氧化应激在MetS编程中起决定性作用。人类和动物研究结果表明,母体来源的损伤会在生命后期诱发MetS,并伴有各种器官系统的氧化应激编程。相反,围产期使用抗氧化剂可以抵消氧化应激,从而预防成年后代的MetS特征。本综述概述了目前关于MetS编程背后核心机制的知识,特别关注与氧化应激相关的发病机制的发生,以及使用潜在的针对氧化应激的干预措施作为一种重新编程策略来避免发育起源的MetS。未来的临床研究应为这些重新编程干预措施预防MetS流行的有效性提供重要的概念验证。