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Review
. 2015 Dec;21(12):973-80.
doi: 10.1016/j.cardfail.2015.09.017. Epub 2015 Oct 3.

Intersections Between Microbiome and Heart Failure: Revisiting the Gut Hypothesis

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Review

Intersections Between Microbiome and Heart Failure: Revisiting the Gut Hypothesis

Yuji Nagatomo et al. J Card Fail. 2015 Dec.

Abstract

Microbes play an important role in human health and disease. In the setting of heart failure (HF), substantial hemodynamic changes, such as hypoperfusion and congestion in the intestines, can alter gut morphology, permeability, function, and possibly the growth and composition of gut microbiota. These changes can disrupt the barrier function of the intestines and exacerbate systemic inflammation via microbial or endotoxin translocation into systemic circulation. Furthermore, cardiorenal alterations via metabolites derived from gut microbiota can potentially mediate or modulate HF pathophysiology. Recently, trimethylamine N-oxide (TMAO) has emerged as a key mediator that provides a mechanistic link between gut microbiota and multiple cardiovascular diseases, including HF. Potential intervention strategies which may target this microbiota-driven pathology include dietary modification, prebiotics/probiotics, and selective binders of microbial enzymes or molecules, but further investigations into their safety and efficacy are warranted.

Keywords: Microbiome; TMAO; heart failure.

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Figures

Figure 1
Figure 1. Interactions between Heart Failure, Gut Microbiota, and Renal Failure
The hemodynamic changes due to heart failure range in microcirculation in intestinal villi. This results in the alterations in intestinal permeability and gut microbiota. Microbial and endotoxin translocation, trimethylamine N-oxide (TMAO), and cardiorenal compromises can mediate the pathology which leads to further exacerbation of heart failure and renal damage. Impaired clearance of these metabolites due to renal dysfunction further promotes this pathology and constitutes a vicious cycle.

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