Abstract
Cardiovascular diseases (CVDs) can originate from early life. Accumulating evidence suggests that gut microbiota in early life is linked to CVDs in later life. Gut microbiota-targeted therapy has gained significant importance in recent decades for its health-promoting role in the prevention (rather than just treatment) of CVDs. Thus far, available gut microbiota-based treatment modalities used as reprogramming interventions include probiotics, prebiotics, and postbiotics. The purpose of this review is, first, to highlight current studies that link dysbiotic gut microbiota to the developmental origins of CVD. This is followed by a summary of the connections between the gut microbiota and CVD behind cardiovascular programming, such as short chain fatty acids (SCFAs) and their receptors, trimethylamine-N-oxide (TMAO), uremic toxins, and aryl hydrocarbon receptor (AhR), and the renin-angiotensin system (RAS). This review also presents an overview of how gut microbiota-targeted reprogramming interventions can prevent the developmental origins of CVD from animal studies. Overall, this review reveals that recent advances in gut microbiota-targeted therapy might provide the answers to reduce the global burden of CVDs. Still, additional studies will be needed to put research findings into practice.
Highlights
Cardiovascular diseases (CVDs), a cluster of disorders of the heart and blood vessels, are the leading cause of death worldwide [1]
Important support for the developmental origins of health and disease (DOHaD) concept came from epidemiological reports following birth cohorts in severe famines, which demonstrated that malnutrition during gestation induced a cluster of CVD risk factors, such as hypertension, dyslipidemia, obesity, kidney disease, type 2 diabetes, and cardiovascular morbidity in adult offspring [4,5]
In view of the fact that a variety of insults during fetal development generates similar cardiovascular outcomes in adulthood, this raises the possibility that a common pathway is involved in the pathogenesis of the developmental origins of CVD
Summary
Cardiovascular diseases (CVDs), a cluster of disorders of the heart and blood vessels, are the leading cause of death worldwide [1]. The developmental origins of health and disease (DOHaD) theory posits that exposure to various insults during critical periods in fetal development leads to structural changes and functional adaption, resulting in increased risk of adult diseases, including CVDs [3]. Important support for the DOHaD concept came from epidemiological reports following birth cohorts in severe famines, which demonstrated that malnutrition during gestation induced a cluster of CVD risk factors, such as hypertension, dyslipidemia, obesity, kidney disease, type 2 diabetes, and cardiovascular morbidity in adult offspring [4,5]. By switching therapy from adulthood to early life before disease occurs, we have the potential to postpone or reduce undesirable programming processes that would lead to CVDs. Over the year, the gut microbiota has gained more attention because, unlike non-modifiable CV risk factors, it can be modified through agents that modulate the intestinal bacterial flora, including prebiotics, probiotics, synbiotics, etc. Hypertension accounts for nearly 80% of searchable publications
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