Abstract
Cardiovascular disease (CVD) presents a global health burden, despite recent advances in management. CVD can originate from early life by so-called “developmental origins of health and disease” (DOHaD). Epidemiological and experimental evidence supports that early-life insults can induce programming of later CVD. Underlying the DOHaD concept, early intervention may offset programming process to prevent the development of CVD, namely reprogramming. Oxidative stress and nutrient sensing signals have been considered to be major mechanisms of cardiovascular programming, while the interplay between these two mechanisms have not been examined in detail. This review summarizes current evidence that supports the link between oxidative stress and nutrient sensing signaling to cardiovascular programming, with an emphasis on the l-arginine–asymmetric dimethylarginine (ADMA)–nitric oxide (NO) pathway. This review provides an overview of evidence from human studies supporting fetal programming of CVD, insight from animal models of cardiovascular programming and oxidative stress, impact of the l-arginine–ADMA–NO pathway in cardiovascular programming, the crosstalk between l-arginine metabolism and nutrient sensing signals, and application of reprogramming interventions to prevent the programming of CVD. A greater understanding of the mechanisms underlying cardiovascular programming is essential to developing early reprogramming interventions to combat the globally growing epidemic of CVD.
Highlights
Cardiovascular disease (CVD) remains a crucial challenge for public health
The developmental origins of health and disease (DOHaD) concept opens a new window in a way that helps to offset the programming process in early life in order to prevent the development of CVD in the later lifespan, through so-called reprogramming [3,6]
This review aims to summarize evidence linking the L-arginine–asymmetric dimethylarginine (ADMA)–nitric oxide (NO) pathway to the development of CVD, with a focus on the interplay between oxidative stress and nutrient sensing signaling, and provide various early manipulations targeting the above mechanisms as a reprogramming approach to prevent the cardiovascular programming and its related comorbidities across the later lifespan
Summary
Cardiovascular disease (CVD) remains a crucial challenge for public health. Despite advances in medical and surgical treatment, CVD still accounts for most noncommunicable disease (NCD) deaths all over the world [1]. Oxidative stress and nutrient sensing signals have been extensively studied individually, the emerging link between these two mechanisms in cardiovascular programming have not been studied in detail. A growing body of evidence from clinical trials and animal studies suggest an impact of ADMA related NO–ROS imbalance on the developmental programming of CVD and cardiovascular outcome [14,19,20,21,22]. This review aims to summarize evidence linking the L-arginine–ADMA–NO pathway to the development of CVD, with a focus on the interplay between oxidative stress and nutrient sensing signaling, and provide various early manipulations targeting the above mechanisms as a reprogramming approach to prevent the cardiovascular programming and its related comorbidities across the later lifespan. NevAersthaelceosnss,etqhueseencheypofotehthesiceasldcoonnsoidt eardavtioocnastecomnocleercnuinlagr wmheacthaisnifsemassibblye worhnicoht winayhuthmeapnhsetnuodtiyesp,e isstugdeaccniaoneermisdmr,aeiaoatenvlmdaimmas. cioAnaudlllsyeamlarsfporcaoohdrmneeensloseoafqtnaycurirpmeeietnaoiscc,lfaewlmcorhiomifitcdiephcetaohldslri,etciavmawnelclphcoeioopc.nrhmIttsaeiisnddntcaeetaenrnla.dtwitsIfityoitnsnohdtsarooecnwwaodsnsiotscyntecporrtenihrtsiieancatoagsmlfofweuonarhcrthcalhaytoaridftsliiomffoeeuvuaraiscnskihscbnuulooelltwafsorolrpemudnrraogoygketrnisapnoemrewohmmgulreismandtmgago,ne seemans dtowcohmateremparoinglryamfromminagnsitmraatlegmyocdaenlsb,ewuhsiecdh. identify how types of early life insults may program cardiovascular phenotypes, which developmental window is critical for cardiovascular programming, and what reprogramming strategy can be used
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