Seminars in Liver Disease,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 29, 2025
Alcohol
is
generally
believed
to
be
metabolized
in
the
liver
by
alcohol
dehydrogenase
(ADH),
aldehyde
(ALDH),
and
a
much
lesser
extent
cytochrome
P450
2E1
(CYP2E1)
other
enzymes.
Recent
studies
suggest
that
gut
also
play
important
roles
promotion
of
metabolism.
ADH,
ALDH,
CYP2E1
have
several
polymorphisms
markedly
impact
These
alcohol-metabolizing
enzymes
not
only
affect
alcohol-associated
disease
(ALD),
but
may
modulate
pathogenesis
diseases
cancer
absence
consumption.
In
this
review,
we
discuss
metabolism
ALD,
metabolic
dysfunction–associated
steatotic
disease,
dysfunction
alcohol–associated
viral
hepatitis,
cancer.
We
how
endogenous
ethanol
production,
affects
Directions
for
future
research
on
are
elaborated.
Journal of Clinical Investigation,
Journal Year:
2024,
Volume and Issue:
134(3)
Published: Feb. 1, 2024
Alcohol-associated
liver
disease
(ALD)
is
a
major
cause
of
chronic
worldwide,
and
comprises
spectrum
several
different
disorders,
including
simple
steatosis,
steatohepatitis,
cirrhosis,
superimposed
hepatocellular
carcinoma.
Although
tremendous
progress
has
been
made
in
the
field
ALD
over
last
20
years,
pathogenesis
remains
obscure,
there
are
currently
no
FDA-approved
drugs
for
treatment
ALD.
In
this
Review,
we
discuss
new
insights
into
therapeutic
targets
ALD,
utilizing
study
multiomics
other
cutting-edge
approaches.
The
potential
translation
these
studies
clinical
practice
therapy
deliberated.
We
also
preclinical
models
interplay
metabolic
dysfunction,
alcohol-associated
cancer,
heterogeneity
some
translational
research
prospects
Journal of Translational Medicine,
Journal Year:
2023,
Volume and Issue:
21(1)
Published: May 4, 2023
Abstract
Alcoholism
is
a
widespread
and
damaging
behaviour
of
people
throughout
the
world.
Long-term
alcohol
consumption
has
resulted
in
alcoholic
liver
disease
(ALD)
being
leading
cause
chronic
disease.
Many
metabolic
enzymes,
including
dehydrogenases
such
as
ADH,
CYP2E1,
CATacetaldehyde
ALDHsand
nonoxidative
metabolizing
enzymes
SULT,
UGT,
FAEES,
are
involved
metabolism
ethanol,
main
component
beverages.
Ethanol
changes
functional
or
expression
profiles
various
regulatory
factors,
kinases,
transcription
microRNAs.
Therefore,
underlying
mechanisms
ALD
complex,
involving
inflammation,
mitochondrial
damage,
endoplasmic
reticulum
stress,
nitrification,
oxidative
stress.
Moreover,
recent
evidence
demonstrated
that
gut-liver
axis
plays
critical
role
pathogenesis.
For
example,
ethanol
damages
intestinal
barrier,
resulting
release
endotoxins
alterations
flora
content
bile
acid
metabolism.
However,
therapies
show
low
effectiveness.
this
review
summarizes
pathways
highly
influential
pathogenic
factors
pathology
with
aim
new
therapeutic
insights.
MedComm,
Journal Year:
2023,
Volume and Issue:
4(1)
Published: Jan. 16, 2023
The
family
of
aldehyde
dehydrogenases
(ALDHs)
contains
19
isozymes
and
is
involved
in
the
oxidation
endogenous
exogenous
aldehydes
to
carboxylic
acids,
which
contributes
cellular
tissue
homeostasis.
ALDHs
play
essential
parts
detoxification,
biosynthesis,
antioxidants,
are
important
value
for
cell
proliferation,
differentiation,
survival
normal
body
tissues.
However,
frequently
dysregulated
associated
with
various
diseases
like
Alzheimer's
disease,
Parkinson's
especially
solid
tumors.
Notably,
involvement
tumor
progression
responsible
maintenance
stem-cell-like
phenotype,
triggering
rapid
aggressive
clinical
progressions.
have
captured
increasing
attention
as
biomarkers
disease
diagnosis
prognosis.
Nevertheless,
these
require
further
longitudinal
studies
large
populations
broad
application.
This
review
summarizes
our
current
knowledge
regarding
potential
tumors
several
non-tumor
diseases,
well
recent
advances
understanding
functions
underlying
molecular
mechanisms
development.
Finally,
we
discuss
therapeutic
therapy
an
emphasis
on
their
implications.
eGastroenterology,
Journal Year:
2023,
Volume and Issue:
1(1), P. e100013 - e100013
Published: Aug. 1, 2023
Excessive
alcohol
drinking
can
cause
pathological
changes
including
carcinogenesis
in
the
digestive
tract
from
mouth
to
large
intestine,
but
underlying
mechanisms
are
not
fully
understood.
In
this
review,
we
discuss
effects
of
on
small
and
intestinal
functions,
such
as
leaky
gut,
dysbiosis
alterations
epithelium
gut
immune
dysfunctions,
commonly
referred
alcohol-associated
bowel
disease
(ABD).
To
date,
detailed
mechanistic
insights
into
ABD
lacking.
Accumulating
evidence
suggests
a
pathogenic
role
ethanol
metabolism
dysfunctions
tract.
Ethanol
generates
acetaldehyde
acetate,
which
could
potentially
promote
functional
disruptions
microbial
host
components
barrier
along
gastrointestinal
The
potential
involvement
acetate
pathogenesis
ABD,
cancer,
is
discussed.
We
also
highlight
some
gaps
knowledge
existing
field
ABD.
Finally,
future
directions
exploring
generated
during
chronic
intake
various
pathologies
affecting
different
sites
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(3), P. 1762 - 1762
Published: Feb. 3, 2022
Aldehyde
dehydrogenases
(ALDHs)
are
the
major
enzyme
superfamily
for
aldehyde
metabolism.
Since
ALDH
polymorphism
leads
to
accumulation
of
acetaldehyde,
we
considered
that
enhancement
liver
activity
by
certain
food
ingredients
could
help
prevent
alcohol-induced
chronic
diseases.
Here,
evaluated
modulating
effects
3-hydroxyphenylacetic
acid
(OPAC),
metabolite
quercetin
glycosides,
on
and
acetaldehyde-induced
cytotoxicity
in
cultured
cell
models.
OPAC
significantly
enhanced
total
not
only
mouse
hepatoma
Hepa1c1c7
cells,
but
also
human
HepG2
cells.
increased
nuclear
level
aryl
hydrocarbon
receptor
(AhR),
AhR-dependent
reporter
gene
expression,
though
factor
erythroid-2-related
2
(Nrf2)-dependent
one.
The
pretreatment
at
concentration
required
upregulation
completely
inhibited
cytotoxicity.
Silencing
AhR
impaired
resistant
effect
against
acetaldehyde.
These
results
strongly
suggested
protects
cells
from
cytotoxicity,
mainly
through
Nrf2-independent
activity.
Our
findings
suggest
has
a
protective
potential
hepatocyte
models
offer
new
preventive
possibility
glycosides
targeting