期刊
BIOMEDICINES
卷 10, 期 4, 页码 -出版社
MDPI
DOI: 10.3390/biomedicines10040875
关键词
developmental origins of health and disease (DOHaD); gut microbiota; hypertension; short chain fatty acid; oxidative stress; probiotics; prebiotics; renin-angiotensin system
资金
- Chang Gung Memorial Hospital, Kaohsiung, Taiwan [CORPG8M0201, CORPG8M0151, CORPG8M0081]
- Ministry of Science and Technology, Taiwan [MOST 110-2314-B-182-020-MY3, MOST 110-2314-B-182A-029]
This review discusses the innovative use of animal models in studying the mechanisms behind developmental origins of hypertension. Research has found that early maternal stress can alter the gut microbiota, leading to adverse outcomes in offspring. Dysbiosis of the gut microbiota is involved in the developmental origins of hypertension, while targeted therapy for the gut microbiota can prevent hypertension in later life.
Hypertension is the leading cause of global disease burden. Hypertension can arise from early life. Animal models are valuable for giving cogent evidence of a causal relationship between various environmental insults in early life and the hypertension of developmental origins in later life. These insults consist of maternal malnutrition, maternal medical conditions, medication use, and exposure to environmental chemicals/toxins. There is a burgeoning body of evidence on maternal insults can shift gut microbiota, resulting in adverse offspring outcomes later in life. Emerging evidence suggests that gut microbiota dysbiosis is involved in hypertension of developmental origins, while gut microbiota-targeted therapy, if applied early, is able to help prevent hypertension in later life. This review discusses the innovative use of animal models in addressing the mechanisms behind hypertension of developmental origins. We will also highlight the application of animal models to elucidate how the gut microbiota connects with other core mechanisms, and the potential of gut microbiota-targeted therapy as a novel preventive strategy to prevent hypertension of developmental origins. These animal models have certainly enhanced our understanding of hypertension of developmental origins, closing the knowledge gap between animal models and future clinical translation.
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