The role of intestinal microbiota in cardiovascular disease

Abstract

Accumulating evidence has indicated that intestinal microbiota is involved in the development of various human diseases, including cardiovascular diseases (CVDs). In the recent years, both human and animal experiments have revealed that alterations in the composition and function of intestinal flora, recognized as gut microflora dysbiosis, can accelerate the progression of CVDs. Moreover, intestinal flora metabolizes the diet ingested by the host into a series of metabolites, including trimethylamine N‐oxide, short chain fatty acids, secondary bile acid and indoxyl sulfate, which affects the host physiological processes by activation of numerous signalling pathways. The aim of this review was to summarize the role of gut microbiota in the pathogenesis of CVDs, including coronary artery disease, hypertension and heart failure, which may provide valuable insights into potential therapeutic strategies for CVD that involve interfering with the composition, function and metabolites of the intestinal flora.

Crosstalk Between the Gut Microbiome and Bioactive Lipids: Therapeutic Targets in Cognitive Frailty

“…Notably, sarcopenia is one of the main conditions involved in the onset of cognitive frailty. Thus, incorporating the Mediterranean diet in the daily habits of patients with cognitive frailty may be a useful strategy for increasing the amount of ω-3 PUFA precursors and, in turn, increasing the availability of anti-inflammatory ω-3 PUFA mediators (e.g., EPA and DHA) (137).…”

The Gut Microbiota in Cardiovascular Disease and Arterial Thrombosis

“…Non-lethal inhibition of gut bacterial TMA lyases with 3,3-dimethyl-1-butanol prevented atherogenesis in Apoe −/− mice on choline rich diet [10,13]. Furthermore, the microbiome-dependent impact of TMAO on prothrombotic platelet function and arterial thrombosis was demonstrated to be transmissible by fecal transplantation from human donors with low or high TMAO-producing microbiota into GF recipient mice [10,88]. Future clinical studies and experimental research need to address the mechanisms through which TMAO influences CVD and arterial thrombosis.…”

“…While choline supplemented diet augmented atherosclerosis and plaque macrophage content in this mouse atherosclerosis study, broad-spectrum antibiotic treatment (0.5 g/L vancomycin, 1 g/L neomycin sulfate, 1 g/L metronidazole, 1 g/L ampicillin) via the drinking water demonstrated that depletion of the microbiota decreased the choline-dependent enhancement of atherosclerotic lesions in male and female Apoe −/− C57BL/6J mice, when kept on a choline-enriched diet at the age of four-weeks until the age of twenty-weeks [16]. Non-lethal inhibition of gut bacterial TMA lyases with 3,3-dimethyl-1-butanol prevented atherogenesis in Apoe −/− mice on choline rich diet [10,13]. Furthermore, the microbiome-dependent impact of TMAO on prothrombotic platelet function and arterial thrombosis was demonstrated to be transmissible by fecal transplantation from human donors with low or high TMAO-producing microbiota into GF recipient mice [10,88].…”

“…The gut microbiota influences the development of vascular inflammation and atherosclerosis [7][8][9]. Various mouse models have shown that intestinal microbial communities have a crucial influence on vascular inflammatory phenotypes, the development of cardiovascular diseases (CVD), and arterial thrombosis [10]. While interfering with host energy metabolism [8], the gut microbiota impacts on the development of atherosclerosis, as demonstrated by the association-based sequencing studies on patient samples [8,[11][12][13] and by the depletion of the gut microbiota with antibiotics or by comparing germ-free (GF) with conventionally raised (CONV-R) mouse atherosclerosis models [7,[13][14][15][16].…”

“…(A) Pro-atherogenic effects are described for the choline-rich diet and the microbiota-derived choline-metabolite trimethylamine N-oxide (TMAO)[12,13,16]. (B) GF Apoe-deficient mice on a chow-diet developed an increased lesion size compared to CONV-R Apoe-deficient mice and the gut microbiota had a cholesterol-lowering function under chow-diet conditions[9,10,14,15].…”