Title:Gut Microbiota and Cardiovascular Disease: Symbiosis Versus
Dysbiosis
Volume: 29
Issue: 23
Author(s): Antonis A. Manolis, Theodora A. Manolis, Helen Melita and Antonis S. Manolis*
Affiliation:
- First
Department of Cardiology, Athens University School of Medicine, Athens, Greece
Keywords:
Microbiome, microbiota, cardiovascular disease, metabolic syndrome, trimethylamine-N-oxide, human GI tract.
Abstract: The gut microbiome interacts with host physiology through various mechanisms,
including the cardiovascular (CV) system. A healthy microbiome has the ability
to process and digest complex carbohydrates into short-chain fatty acids (SCFA). These
SCFA function as signaling molecules, immune-modulating molecules, and energy
sources. However, when the microbiome is altered, it produces gut dysbiosis with overgrowth
of certain bacteria that may lead to overproduction of trimethylamine-N-oxide (TMAO)
from the metabolism of phosphatidylcholine, choline, and carnitine; dysbiosis also
leads to increased intestinal permeability allowing the microbiome-derived
lipopolysaccharide (LPS), a bacterial endotoxin, to enter the blood circulation, triggering
inflammatory responses. An altered gastrointestinal (GI) tract environment and microbiome-
derived metabolites are associated with CV events. Disrupted content and function
of the microbiome leading to elevated TMAO and LPS levels, altered bile acid
metabolism pathways, and SCFA production are associated with an increased risk of CV
diseases (CVD), including atherosclerosis, myocardial infarction, thrombosis, arrhythmias,
and stroke. Therapeutic interventions that may favorably influence a dysbiotic GI
tract profile and promote a healthy microbiome may benefit the CV system and lead to a
reduction of CVD incidence in certain situations. These issues are herein reviewed with a
focus on the spectrum of microbiota-related CVD, the mechanisms involved, and the potential
use of microbiome modification as a possible therapeutic intervention.
