Protein & Cell,
Journal Year:
2018,
Volume and Issue:
9(5), P. 416 - 431
Published: May 1, 2018
Trillions
of
microbes
inhabit
the
human
gut,
not
only
providing
nutrients
and
energy
to
host
from
ingested
food,
but
also
producing
metabolic
bioactive
signaling
molecules
maintain
health
elicit
disease,
such
as
cardiovascular
disease
(CVD).
CVD
is
leading
cause
mortality
worldwide.
In
this
review,
we
presented
gut
microbiota
derived
metabolites
involved
in
including
trimethylamine-N-oxide
(TMAO),
uremic
toxins,
short
chain
fatty
acids
(SCFAs),
phytoestrogens,
anthocyanins,
bile
lipopolysaccharide.
These
play
critical
roles
maintaining
a
healthy
function,
if
dysregulated,
potentially
causally
linked
CVD.
A
better
understanding
function
dynamics
holds
great
promise
toward
mechanistic
predicative
biomarker
discoveries
precise
interventions.
Circulation Research,
Journal Year:
2017,
Volume and Issue:
120(7), P. 1183 - 1196
Published: March 30, 2017
Significant
interest
in
recent
years
has
focused
on
gut
microbiota-host
interaction
because
accumulating
evidence
revealed
that
intestinal
microbiota
play
an
important
role
human
health
and
disease,
including
cardiovascular
diseases.
Changes
the
composition
of
associated
with
referred
to
as
dysbiosis,
have
been
linked
pathologies
such
atherosclerosis,
hypertension,
heart
failure,
chronic
kidney
obesity,
type
2
diabetes
mellitus.
In
addition
alterations
composition,
metabolic
potential
identified
a
contributing
factor
development
Recent
studies
can
elicit
variety
effects
host.
Indeed,
microbiome
functions
like
endocrine
organ,
generating
bioactive
metabolites,
impact
host
physiology.
Microbiota
interact
through
many
pathways,
trimethylamine/trimethylamine
Nature Communications,
Journal Year:
2017,
Volume and Issue:
8(1)
Published: Oct. 4, 2017
The
gut
microbiota
has
been
linked
to
cardiovascular
diseases.
However,
the
composition
and
functional
capacity
of
microbiome
in
relation
diseases
have
not
systematically
examined.
Here,
we
perform
a
metagenome-wide
association
study
on
stools
from
218
individuals
with
atherosclerotic
disease
(ACVD)
187
healthy
controls.
ACVD
deviates
status
by
increased
abundance
Enterobacteriaceae
Streptococcus
spp.
and,
functionally,
potential
for
metabolism
or
transport
several
molecules
important
health.
Although
drug
treatment
represents
confounding
factor,
status,
current
use,
is
major
distinguishing
feature
this
cohort.
We
identify
common
themes
comparison
data
associated
other
cardiometabolic
(obesity
type
2
diabetes),
liver
cirrhosis,
rheumatoid
arthritis.
Our
represent
comprehensive
resource
further
investigations
role
promoting
preventing
as
well
related
diseases.The
may
play
authors
controls,
identifying
microbial
strains
functions
disease.
Circulation Research,
Journal Year:
2014,
Volume and Issue:
116(3), P. 448 - 455
Published: Nov. 7, 2014
Trimethylamine-N-oxide
(TMAO),
a
gut
microbial-dependent
metabolite
of
dietary
choline,
phosphatidylcholine
(lecithin),
and
l-carnitine,
is
elevated
in
chronic
kidney
diseases
(CKD)
associated
with
coronary
artery
disease
pathogenesis.To
both
investigate
the
clinical
prognostic
value
TMAO
subjects
versus
without
CKD,
test
hypothesis
that
plays
direct
contributory
role
development
progression
renal
dysfunction.We
first
examined
relationship
between
fasting
plasma
all-cause
mortality
over
5-year
follow-up
521
stable
CKD
(estimated
glomerular
filtration
rate,
<60
mL/min
per
1.73
m(2)).
Median
level
among
was
7.9
μmol/L
(interquartile
range,
5.2-12.4
μmol/L),
which
markedly
higher
(P<0.001)
than
non-CKD
(n=3166).
Within
subjects,
(fourth
quartile)
2.8-fold
increased
risk.
After
adjustments
for
traditional
risk
factors,
high-sensitivity
C-reactive
protein,
estimated
levels
remained
predictive
(hazard
ratio,
1.93;
95%
confidence
interval,
1.13-3.29;
P<0.05).
provided
significant
incremental
(net
reclassification
index,
17.26%;
P<0.001
differences
area
under
receiver
operator
characteristic
curve,
63.26%
65.95%;
P=0.036).
Among
portend
poorer
prognosis
within
cohorts
high
low
cystatin
C.
In
animal
models,
choline
or
directly
led
to
progressive
tubulointerstitial
fibrosis
dysfunction.Plasma
are
patients
long-term
survival.
Chronic
exposures
increase
contributes
dysfunction
models.
Journal of the American Heart Association,
Journal Year:
2016,
Volume and Issue:
5(2)
Published: Feb. 23, 2016
Background
The
choline‐derived
metabolite
trimethylamine
N‐oxide
(
TMAO
)
has
been
demonstrated
to
contribute
atherosclerosis
and
is
associated
with
coronary
artery
disease
risk.
Methods
Results
We
explored
the
impact
of
on
endothelial
smooth
muscle
cell
function
in
vivo,
focusing
disease‐relevant
outcomes
for
atherogenesis.
Initially,
we
observed
that
aortas
LDLR
−/−
mice
fed
a
choline
diet
showed
elevated
inflammatory
gene
expression
compared
controls.
Acute
injection
at
physiological
levels
was
sufficient
induce
same
markers
activate
well‐known
mitogen‐activated
protein
kinase,
extracellular
signal–related
nuclear
factor‐κB
signaling
cascade.
These
observations
were
recapitulated
primary
human
aortic
cells
vascular
cells.
also
found
promotes
recruitment
activated
leukocytes
Through
pharmacological
inhibition,
further
activation
necessary
both
these
relevant
types
as
well
adhesion
leukocytes.
Conclusions
Our
results
suggest
likely
contributory
mechanism
‐dependent
enhancement
cardiovascular
risks.
Circulation Research,
Journal Year:
2020,
Volume and Issue:
127(4), P. 553 - 570
Published: July 30, 2020
Fecal
microbial
community
changes
are
associated
with
numerous
disease
states,
including
cardiovascular
(CVD).
However,
such
data
merely
associative.
A
causal
contribution
for
gut
microbiota
in
CVD
has
been
further
supported
by
a
multitude
of
more
direct
experimental
evidence.
Indeed,
transplantation
studies,
specific
microbiota-dependent
pathways,
and
downstream
metabolites
have
all
shown
to
influence
host
metabolism
CVD,
sometimes
through
identified
receptors.
Multiple
metaorganismal
pathways
(involving
both
microbe
host)
impact
animal
models
show
striking
clinical
associations
human
studies.
For
example,
trimethylamine
N-oxide
and,
recently,
phenylacetylglutamine
whose
blood
levels
incident
risks
large-scale
Importantly,
link
these
other
metabolites/pathways
mechanistic
model
Phenylacetylglutamine,
was
recently
promote
adverse
phenotypes
the
via
interaction
multiple
ARs
(adrenergic
receptors)-a
class
key
receptors
that
regulate
homeostasis.
In
this
review,
we
summarize
recent
advances
microbiome
research
related
cardiometabolic
helped
move
field
forward
from
associative
causative
results.
We
focus
on
compounds/pathways,
attention
paid
short-chain
fatty
acids,
secondary
bile
N-oxide,
phenylacetylglutamine.
also
discuss
novel
therapeutic
strategies
directly
targeting
improve
outcomes.
