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REVIEW ARTICLE
Gut Microbiota and Cardiovascular Disease: Symbiosis Versus
Dysbiosis
Antonis A. Manolis
1
, Theodora A. Manolis
2
, Helen Melita
3
and Antonis S. Manolis
4,*
1
Patras University School of Medicine, Patras, Greece;
2
Aiginiteio University Hospital, Athens, Greece;
3
Onassis Cardiac Surgery Center, Athens, Greece;
4
Athens University School of Medicine, Athens, Greece
ARTICLE HISTORY
Received: August 03, 2021
Revised: October 28, 2021
Accepted: October 31, 2021
DOI:
10.2174/0929867328666211213112949
Abstract: The gut microbiome interacts with host physiology through various mech-
anisms, 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 over-
growth of certain bacteria that may lead to overproduction of trimethylamine-N-oxide (T-
MAO) from the metabolism of phosphatidylcholine, choline, and carnitine; dysbiosis al-
so 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 micro-
biome-derived metabolites are associated with CV events. Disrupted content and func-
tion 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, arrhyth-
mias, 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 po-
tential use of microbiome modification as a possible therapeutic intervention.
Keywords: Microbiome, microbiota, cardiovascular disease, metabolic syndrome, trimethylamine-N-oxide.
1. INTRODUCTION
Cardiovascular (CV) disease (CVD) is currently the
leading global cause of death [1]. In addition to several
other conditions known to cause CVD, alterations to
the gut microbiome have recently been shown to pro-
mote CVD [2-5].
The human microbiome of the gastrointestinal (GI)
tract encompasses over 100 trillion microbial cells and
100 different bacterial species, a crucial symbiosis that
greatly impacts host homeostasis, maintaining the phy-
siological and metabolic health of the host [6]. Consid-
erable knowledge of the human microbiome was ac-
quired after 2007, the year the Human Microbiome Pro-
ject was launched, a 5-year-long international effort
*Address correspondence to this author at the First Department of
Cardiology, Hippokrateio Hospital, Vas. Sofias 114, Athens 115
27, Greece; E-mail: asm@otenet.gr
to characterize the microbial populations found in the
human body and to identify each microorganism’s role
in health and disease [7, 8].
Although the consistency of the microbiome may
vary in each human GI tract, obligate anaerobes out-
number facultative anaerobes and aerobes by up to
100-fold; over 90% of bacteria in a healthy adult GI
tract consists of the Bacteroidetes (especially the gen-
era Bacteroides and Prevotella) and Firmicutes phyla
(especially members of the genus Clostridium); minor
phyla include Actinobacteria, Proteobacteria, and Ver-
rucomicrobia, and methanogens as the dominant
amongst the Archaea; some fungi, and viruses are also
present (Table 1). Specifically, 8 abundant genera,
comprising Bacteroides, Eubacterium, Faecalibacteri-
um, Alistipes, Ruminococcus, Clostridium, Roseburia,
and Blautia, were identified in more than 1000 humans
[9, 10]. These microorganisms all aid in digestion, but
they can also produce valuable nutrients; lactic acid