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Interplay between Oxidative Stress and Nutrient Sensing Signaling in the Developmental Origins of Cardiovascular
You-Lin Tain1,2, Chien-Ning Hsu3,4
1Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan. tainyl@hotmail.com.
Insights
Early life factors can program cardiovascular disease (CVD) risk. Interventions targeting oxidative stress and nutrient sensing pathways, like the l-arginine-nitric oxide pathway, may prevent CVD development.
Area of Science:
- Cardiovascular Research
- Developmental Biology
- Nutritional Science
Background:
- Cardiovascular disease (CVD) is a major global health issue.
- The "developmental origins of health and disease" (DOHaD) concept suggests early-life insults can program later CVD.
- Interventions during early life, termed "reprogramming," may prevent CVD.
Purpose of the Study:
- To review the link between oxidative stress and nutrient sensing signaling in cardiovascular programming.
- To emphasize the role of the l-arginine-asymmetric dimethylarginine (ADMA)-nitric oxide (NO) pathway.
- To explore reprogramming interventions for CVD prevention.
Main Methods:
- Review of human studies on fetal programming of CVD.
- Analysis of animal models of cardiovascular programming and oxidative stress.
- Examination of the l-arginine-ADMA-NO pathway and its crosstalk with nutrient sensing signals.
Main Results:
- Evidence supports early-life insults programming CVD.
- Oxidative stress and nutrient sensing are key mechanisms.
- The l-arginine-ADMA-NO pathway is critical in cardiovascular programming.
- Crosstalk exists between l-arginine metabolism and nutrient sensing.
Conclusions:
- Understanding cardiovascular programming mechanisms is crucial.
- Early reprogramming interventions are essential to combat the CVD epidemic.
- Targeting oxidative stress and nutrient sensing offers therapeutic potential.
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.