Neurobiology of Disease,
Год журнала:
2024,
Номер
192, С. 106423 - 106423
Опубликована: Янв. 28, 2024
Trimethylamine-N-oxide
(TMAO)
is
a
gut
microbiota-derived
metabolite
produced
by
the
action
of
microbiota
and
hepatic
enzyme
Flavin
Mono‑oxygenase
3
(FMO3).
TMAO
level
has
positive
correlation
with
risk
cardiovascular
events,
including
stroke,
their
influenced
mainly
dietary
choice
liver
FMO3.
plays
role
in
development
atherosclerosis
plaque,
which
one
causative
factors
stroke
event.
Preclinical
clinical
investigations
on
associated
risk,
severity,
outcomes
are
summarised
this
review.
In
addition,
mechanisms
TMAO-driven
vascular
dysfunction
also
discussed,
such
as
inflammation,
oxidative
stress,
thrombus
foam
cell
formation,
altered
cholesterol
bile
acid
metabolism,
etc.
Post-stroke
inflammatory
cascades
involving
activation
immune
cells,
i.e.,
microglia
astrocytes,
result
Blood-brain-barrier
(BBB)
disruption,
allowing
to
infiltrate
brain
further
aggravate
inflammation.
This
event
occurs
NOD-like
receptor
family
pyrin
domain
containing
(NLRP3)
inflammasome
pathway
through
release
cytokines
chemokines
that
BBB
initiate
recruitment
cells
brain.
Thus,
it's
likely
maintaining
levels
could
be
promising
approach
for
treating
improving
complications.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(11), С. 6188 - 6188
Опубликована: Июнь 4, 2024
Chronic
inflammation
drives
the
growth
of
colorectal
cancer
through
dysregulation
molecular
pathways
within
immune
system.
Infiltration
cells,
such
as
macrophages,
into
tumoral
regions
results
in
release
proinflammatory
cytokines
(IL-6;
IL-17;
TNF-α),
fostering
tumor
proliferation,
survival,
and
invasion.
Tumors
employ
various
mechanisms
to
evade
surveillance,
effectively
‘cloaking’
themselves
from
detection
subsequent
attack.
A
comprehensive
understanding
these
intricate
interactions
is
paramount
for
advancing
novel
strategies
aimed
at
modulating
response
against
cancer.
Frontiers in Immunology,
Год журнала:
2024,
Номер
14
Опубликована: Янв. 15, 2024
Inflammatory
bowel
disease
(IBD),
characterized
primarily
by
gastrointestinal
inflammation,
predominantly
manifests
as
Crohn’s
(CD)
and
ulcerative
colitis
(UC).
It
is
acknowledged
that
Inflammation
plays
a
significant
role
in
cancer
development
patients
with
IBD
have
an
increased
risk
of
various
cancers.
The
progression
from
inflammation
to
carcinogenesis
result
the
interplay
between
immune
cells,
gut
microbiota,
carcinogenic
signaling
pathways
epithelial
cells.
Long-term
chronic
can
lead
accumulation
mutations
cells
abnormal
activation
pathways.
Furthermore,
Immune
play
pivotal
both
acute
phases
IBD,
contributing
transformation
tumorigenesis.
And
frequently
exhibit
dysbiosis
intestinal
microbiome.
Disruption
microbiota
subsequent
dysregulation
are
central
pathogenesis
associated
colorectal
(CAC).
proactive
management
combined
regular
endoscopic
tumor
screenings
represents
most
direct
effective
strategy
prevent
IBD-associated
cancer.
Scientific Reports,
Год журнала:
2024,
Номер
14(1)
Опубликована: Март 8, 2024
Abstract
This
study
examined
the
interplay
between
bacterial
and
fungal
communities
in
human
gut
microbiota,
impacting
on
nutritional
status
body
weight.
Cohorts
of
10
participants
healthy
weight,
overweight,
obese
individuals,
underwent
comprehensive
analysis,
including
dietary,
anthropometric,
biochemical
evaluations.
Microbial
composition
was
studied
via
gene
sequencing
16S
ITS
rDNA
regions,
revealing
(bacteriota)
(mycobiota)
profiles.
Bacterial
diversity
exceeded
diversity.
Statistically
significant
differences
were
found
within
healthy-weight,
groups.
The
Bacillota/Bacteroidota
ratio
(previously
known
as
Firmicutes/Bacteroidetes
ratio)
correlated
positively
with
mass
index.
predominant
phyla
Ascomycota
Basidiomycota,
genera
Nakaseomyces
,
Kazachstania
Kluyveromyces
Hanseniaspora
inversely
correlating
weight
gain;
while
Saccharomyces
Debaryomyces
Pichia
Overweight
individuals
who
harbored
a
higher
abundance
Akkermansia
muciniphila,
demonstrated
favorable
lipid
glucose
profiles
contrast
to
those
lower
abundance.
overweight
group
had
elevated
Candida
linked
simple
carbohydrate
consumption.
underscores
role
microbial
taxa
index
metabolic
health.
An
imbalanced
bacteriota/mycobiota
may
contribute
obesity/metabolic
disorders,
highlighting
significance
investigating
both
communities.
The
human
microbiome,
particularly
the
gut
has
emerged
as
a
central
determinant
of
health
and
disease.
Dysbiosis,
an
imbalance
in
microbial
composition
gut,
is
associated
with
variety
metabolic
other
diseases,
highlighting
potential
for
microbiota-targeted
treatments.
Fecal
microbiota
transplantation
received
considerable
attention
promising
therapy
to
modulate
microbiome
restore
homeostasis.
However,
challenges
remain,
including
standardization,
safety,
long-term
efficacy.
This
review
summarizes
current
knowledge
on
fecal
describes
next
generation
therapies
targeting
microbiome.
looked
at
mechanistic
understanding
alternative
strategies,
elucidating
their
role
improving
dysbiosis-associated
disorders,
such
obesity,
type
2
diabetes
others.
Additionally,
this
discussed
growing
application
Insights
from
clinical
trials,
preclinical
studies,
emerging
technologies
provide
comprehensive
overview
evolving
landscape
microbiome-based
interventions.
Through
critical
assessment
advances
prospects,
aims
highlight
therapeutic
pave
way
innovative
approaches
precision
medicine
personalized
Neurobiology of Disease,
Год журнала:
2024,
Номер
192, С. 106423 - 106423
Опубликована: Янв. 28, 2024
Trimethylamine-N-oxide
(TMAO)
is
a
gut
microbiota-derived
metabolite
produced
by
the
action
of
microbiota
and
hepatic
enzyme
Flavin
Mono‑oxygenase
3
(FMO3).
TMAO
level
has
positive
correlation
with
risk
cardiovascular
events,
including
stroke,
their
influenced
mainly
dietary
choice
liver
FMO3.
plays
role
in
development
atherosclerosis
plaque,
which
one
causative
factors
stroke
event.
Preclinical
clinical
investigations
on
associated
risk,
severity,
outcomes
are
summarised
this
review.
In
addition,
mechanisms
TMAO-driven
vascular
dysfunction
also
discussed,
such
as
inflammation,
oxidative
stress,
thrombus
foam
cell
formation,
altered
cholesterol
bile
acid
metabolism,
etc.
Post-stroke
inflammatory
cascades
involving
activation
immune
cells,
i.e.,
microglia
astrocytes,
result
Blood-brain-barrier
(BBB)
disruption,
allowing
to
infiltrate
brain
further
aggravate
inflammation.
This
event
occurs
NOD-like
receptor
family
pyrin
domain
containing
(NLRP3)
inflammasome
pathway
through
release
cytokines
chemokines
that
BBB
initiate
recruitment
cells
brain.
Thus,
it's
likely
maintaining
levels
could
be
promising
approach
for
treating
improving
complications.
