Far from the eyes, close to the heart: dysbiosis of gut microbiota and cardiovascular consequences

Abstract

These days, the gut microbiota is universally recognized as an active organ that can modulate the overall host metabolism by promoting multiple functions, from digestion to the systemic maintenance of overall host physiology. Dysbiosis, the alteration of the complex ecologic system of gut microbes, is associated with and causally responsible for multiple types of pathologies. Among the latters, metabolic diseases such as type 2 diabetes and obesity are each distinguishable by a unique gut microbiota profile. Interestingly, the specific microbiota typically found in the blood of diabetic patients also has been observed at the level of atherosclerotic plaque. Here, we report evidence from the literature, as well as a few controversial reports, regarding the putative role of gut microbiota dysbiosis-induced cardiovascular diseases, such as atherosclerosis, which are common comorbidities of metabolic dysfunction.

Fig. 1

Gut microbiota and its impact on the cardiovascular system. Products from a protein-rich diet, such as L-carnitine and phosphatidylcholine, may be metabolized into choline, which is converted to trimethylamine (TMA) by the gut microbiota. TMA may be oxidized into the liver to form TMA-N-oxide (TMAO), which can promote the formation of atherosclerotic plaque [••]. On the other hand, diet-induced gut microbiota dysbiosis may result in bacterial translocation into the systemic blood flow, where a blood microbiota (almost 90 % Gram-negative bacteria) may become established [••]. Subsequently, atherosclerotic plaques may develop and promote atherosclerosis and cardiovascular diseases. Interestingly, a plaque-specific blood-like microbiota exists, and it is dominated by Gram-negative bacteria (Proteobacteria phylum) as well [39]