Annals of Hepatology,
Год журнала:
2025,
Номер
unknown, С. 101896 - 101896
Опубликована: Март 1, 2025
Liver
fibrosis
is
a
progressive
response
to
chronic
liver
diseases
characterized
by
wound-healing
process
that
leads
the
accumulation
of
fibrillary
extracellular
matrix
(ECM)
proteins
in
and
around
tissue.
If
left
untreated,
can
advance
cirrhosis
ultimately
result
failure.
Although
there
have
been
significant
advancements
understanding
molecular
mechanisms
involved
fibrosis,
effective
therapeutic
strategies
reverse
or
halt
condition
remain
limited.
Recent
research
has
underscored
critical
role
energy
metabolism
initiation
progression
fibrosis.
In
injury,
hepatic
cells
undergo
metabolic
reprogramming
meet
demands
myofibroblasts.
This
involves
various
changes,
including
mitochondrial
dysfunction,
alterations
cellular
bioenergetics,
shifts
glycolysis
oxidative
phosphorylation,
as
well
changes
lipid
metabolism.
These
modifications
disrupt
homeostasis
increase
release,
activating
cells,
primarily
stellate
(HSCs).
Activated
HSCs
then
stimulate
fibrogenic
pathways,
leading
ECM
liver,
which
exacerbates
review
aims
explore
emerging
connection
between
focusing
on
drive
this
condition.
We
also
examine
implications
modulating
reduce
release
mitigate
Altering
decrease
may
represent
promising
approach
for
treating
diseases.
Journal of Hepatology,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 1, 2025
The
liver
acts
as
a
central
metabolic
hub,
integrating
signals
from
the
gastrointestinal
tract
and
adipose
tissue
to
regulate
carbohydrate,
lipid,
amino
acid
metabolism.
Gut-derived
metabolites,
such
acetate
ethanol
non-esterified
fatty
acids
white
(WAT),
influence
hepatic
processes,
which
rely
on
mitochondrial
function
maintain
systemic
energy
balance.
Metabolic
dysregulation
obesity,
insulin
resistance,
type
2
diabetes
disrupt
these
pathways,
leading
dysfunction-associated
steatotic
disease
(MASLD)
steatohepatitis
(MASH).
This
review
explores
fluxes
within
gut-adipose
tissue-liver
axis,
focusing
pivotal
role
of
de
novo
lipogenesis
(DNL),
dietary
substrates
like
glucose
fructose,
changes
in
during
MASLD
progression.
It
highlights
contributions
resistance
impaired
dynamics
lipid
accumulation.
Further
understanding
how
interplay
between
substrate
flux
gastro-intestinal
integrates
with
intersects
structural
functional
alterations
mitochondria
will
be
important
identify
novel
therapeutic
targets
advance
treatment
MASH.
Lipids in Health and Disease,
Год журнала:
2024,
Номер
23(1)
Опубликована: Апрель 2, 2024
Abstract
Metabolic
dysfunction-associated
steatotic
liver
disease
(MASLD)
is
the
leading
cause
of
chronic
that
affects
over
30%
world’s
population.
For
decades,
heterogeneity
non-alcoholic
fatty
(NAFLD)
has
impeded
our
understanding
mechanism
and
development
effective
medications.
However,
a
recent
change
in
nomenclature
from
NAFLD
to
MASLD
emphasizes
critical
role
systemic
metabolic
dysfunction
pathophysiology
this
therefore
promotes
progress
pharmaceutical
treatment
MASLD.
In
review,
we
focus
on
underlying
abnormality
hepatic
lipid
metabolism
patients
with
MASLD,
summarize
latest
therapeutic
medications
target
disorders.
Frontiers in Immunology,
Год журнала:
2024,
Номер
15
Опубликована: Янв. 17, 2024
Metabolic
dysfunction-associated
steatohepatitis
(MASH)
is
the
replacement
term
for
what
used
to
be
called
nonalcoholic
(NASH).
It
characterized
by
inflammation
and
injury
of
liver
in
presence
cardiometabolic
risk
factors
may
eventually
result
development
hepatocellular
carcinoma
(HCC),
most
common
form
primary
cancer.
Several
pathogenic
mechanisms
are
involved
transition
from
MASH
HCC,
encompassing
metabolic
injury,
inflammation,
immune
dysregulation
fibrosis.
In
this
context,
Gas6
(Growth
Arrest-Specific
6)
TAM
(Tyro3,
Axl,
MerTK)
receptors
play
important
roles.
The
Gas6/TAM
family
modulation
lipid
metabolism,
fibrosis,
tumor
progression
metastasis,
processes
which
an
role
pathophysiology
acute
chronic
diseases.
review,
we
discuss
MASH-associated
HCC
potential
involvement
system
disease
progression.
addition,
since
therapeutic
strategies
limited,
also
speculate
regarding
possible
future
treatments
involving
targeting
or
receptors.
Trends in Pharmacological Sciences,
Год журнала:
2024,
Номер
45(4), С. 319 - 334
Опубликована: Март 12, 2024
Steatotic
liver
diseases
(SLDs)
affect
one-third
of
the
population,
but
pathogenesis
underlying
these
is
not
well
understood,
limiting
available
treatments.
A
common
factor
in
SLDs
increased
hepatic
mitochondrial
reductive
stress,
which
occurs
as
a
result
excessive
lipid
and
alcohol
metabolism.
Recent
research
has
also
shown
that
genetic
risk
factors
contribute
to
this
stress.
This
review
aims
explore
how
increase
stress
it
disrupts
metabolism,
leading
SLDs.
Additionally,
will
discuss
latest
clinical
studies
on
pharmaceutical
treatments
for
SLDs,
specifically
peroxisome
proliferator-activated
receptor
gamma
(PPAR-γ)
agonists,
thyroid
hormone
(THR)
acetyl-CoA
carboxylase
(ACC)
inhibitors,
uncouplers.
These
have
effect
decreasing
been
largely
overlooked.
Clinical and Molecular Hepatology,
Год журнала:
2024,
Номер
unknown
Опубликована: Авг. 5, 2024
Metabolic
dysfunction-associated
steatotic
liver
disease
(MASLD)
is
a
complex
multifactorial
and
becoming
the
leading
cause
of
liver-related
morbidity
mortality.
MASLD
spans
from
isolated
steatosis
to
metabolic
steatohepatitis
(MASH),
that
may
progress
cirrhosis
hepatocellular
carcinoma
(HCC).
Genetic,
metabolic,
environmental
factors
strongly
contribute
heterogeneity
MASLD.
Lifestyle
intervention
weight
loss
represent
viable
treatment
for
Moreover,
Resmetirom,
thyroid
hormone
beta
receptor
agonist,
has
recently
been
approved
treatment.
However,
most
individuals
treated
did
not
respond
this
therapeutic
suggesting
need
more
tailored
approach
treat
Oligonucleotide-based
therapies,
namely
small-interfering
RNA
(siRNA)
antisense
oligonucleotide
(ASO),
have
developed
tackle
by
reducing
expression
genes
influencing
MASH
progression,
such
as
PNPLA3
HSD17B13.
Here,
we
review
latest
made
in
synthesis
development
oligonucleotide-based
agents
targeting
genetic
determinants
MASH.
