Abstract
Increasing evidence suggests that fetal programming through environmental exposure during a critical window of early life leads to long-term detrimental outcomes, by so-called developmental origins of health and disease (DOHaD). Hypertension can originate in early life. Animal models are essential for providing convincing evidence of a causal relationship between diverse early-life insults and the developmental programming of hypertension in later life. These insults include nutritional imbalances, maternal illnesses, exposure to environmental chemicals, and medication use. In addition to reviewing the various insults that contribute to hypertension of developmental origins, this review focuses on the benefits of animal models in addressing the underlying mechanisms by which early-life interventions can reprogram disease processes and prevent the development of hypertension. Our understanding of hypertension of developmental origins has been enhanced by each of these animal models, narrowing the knowledge gap between animal models and future clinical translation.
Highlights
The findings suggest that the interplay between the renin–angiotensin system (RAS) and other mechanisms in early life is implicated in renal programming and hypertension in adulthood
Our prior studies reported that maternal consumption of a high-fructose or high-fat diet induced hypertension in adult offspring, which can be prevented by modulating the gut microbiota through the intake of prebiotic inulin or probiotic Lactobacillus casei [127,128]
Given the advances in our understanding of the developmental origins of health and disease (DOHaD) research field, it has become apparent that early-life interventions can reprogram molecular mechanisms behind hypertension of developmental origins to prevent the development of hypertension in adulthood
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The DOHaD hypothesis gained momentum after the emergence of observational studies from the 1944–1945 Dutch famine cohort, illustrating that maternal starvation is associated with an increased risk of metabolic and cardiovascular diseases in adult offspring [3]. These findings, combined with numerous subsequent epidemiologic investigations, indicate that the perinatal period, a critical window of organogenesis, is a vulnerable time in terms of the impact of adverse environmental insults [4].
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