Abstract
Nonalcoholic
fatty
liver
disease
(NAFLD)
encompasses
a
broad
range
of
conditions,
commencing
with
simple
steatosis
and
progressing
to
non‐alcoholic
steatohepatitis,
the
possibility
further
deterioration
into
fibrosis,
cirrhosis,
ultimately,
hepatocellular
carcinoma.
Unfortunately,
there
is
currently
no
approved
medication
for
treating
NAFLD‐associated
steatosis.
This
underscores
need
improved
therapeutic
approaches
that
can
modulate
lipid
metabolism
halt
transition
from
chronic
disease.
Our
previous
studies
have
demonstrated
apoptotic
vesicles
(apoVs),
which
are
produced
during
apoptosis,
show
great
potential
in
regulating
homeostasis.
However,
whether
they
ameliorate
NAFLD
unknown.
In
our
research,
apoVs
derived
platelets
(PLT‐apoVs)
as
well
mesenchymal
stem
cells
(MSC‐apoVs)
were
used
treat
NAFLD.
The
results
showed
PLT‐apoVs
exhibited
superior
effects
diminishing
accumulation
induced
by
high‐fat
diet
than
MSC‐apoVs.
Through
proteomic
analysis,
we
defined
validated
apolipoprotein
A‐II
(APOA2)
regulator
apoV‐mediated
MSC
adipogenesis,
could
be
target
enhance
apoV
biomedical
field.
Owing
higher
expression
APOA2,
better
pave
way
apoV‐based
therapy
Gut,
Год журнала:
2024,
Номер
unknown, С. gutjnl - 330595
Опубликована: Янв. 16, 2024
Non-alcoholic
fatty
liver
disease
(NAFLD)
has
rapidly
become
the
most
common
chronic
globally
and
is
currently
estimated
to
affect
up
38%
of
global
adult
population.
NAFLD
a
multisystem
where
systemic
insulin
resistance
related
metabolic
dysfunction
play
pathogenic
role
in
development
its
relevant
liver-related
morbidities
(cirrhosis,
failure
hepatocellular
carcinoma)
extrahepatic
complications,
such
as
cardiovascular
(CVD),
type
2
diabetes
mellitus,
kidney
disease,
certain
types
cancers.
In
2023,
three
large
multinational
associations
proposed
that
dysfunction-associated
steatotic
(MASLD)
should
replace
term
NAFLD;
name
chosen
non-alcoholic
steatohepatitis
was
(MASH).
Emerging
epidemiological
evidence
suggests
an
excellent
concordance
rate
between
MASLD
definitions—that
is,
~99%
individuals
with
meet
criteria.
this
narrative
review,
we
provide
overview
literature
on
(a)
recent
data
risk
developing
CVD
malignant
(b)
underlying
mechanisms
by
which
(and
factors
strongly
linked
MASLD)
may
increase
these
complications
(c)
diagnosis
assessment
potential
treatments
reduce
people
or
MASH.
Cell Metabolism,
Год журнала:
2024,
Номер
36(7), С. 1439 - 1455
Опубликована: Май 31, 2024
Chronic
liver
diseases,
primarily
metabolic
dysfunction-associated
steatotic
disease
(MASLD),
harmful
use
of
alcohol,
or
viral
hepatitis,
may
result
in
fibrosis,
cirrhosis,
and
cancer.
Hepatic
fibrogenesis
is
a
complex
process
with
interactions
between
different
resident
non-resident
heterogeneous
cell
populations,
ultimately
leading
to
deposition
extracellular
matrix
organ
failure.
Shifts
phenotypes
functions
involve
pronounced
transcriptional
protein
synthesis
changes
that
require
adaptations
cellular
substrate
metabolism,
including
glucose
lipid
resembling
associated
the
Warburg
effect
cancer
cells.
Cell
activation
are
regulated
by
stress
responses,
unfolded
response,
endoplasmic
reticulum
stress,
autophagy,
ferroptosis,
nuclear
receptor
signaling.
These
crucial
for
inflammatory
fibrogenic
macrophages,
lymphoid
cells,
hepatic
stellate
Modulation
these
pathways,
therefore,
offers
opportunities
novel
therapeutic
approaches
halt
even
reverse
fibrosis
progression.
Molecular Aspects of Medicine,
Год журнала:
2023,
Номер
95, С. 101231 - 101231
Опубликована: Дек. 5, 2023
Liver
fibrosis,
as
an
excess
deposition
of
extracellular
matrix
(ECM)
components,
results
from
chronic
liver
injury
well
persistent
activation
inflammatory
response
and
fibrogenesis.
fibrosis
is
a
major
determinant
for
disease
(CLD)
progression
in
the
last
two
decades
our
understanding
on
molecular
cellular
mechanisms
underlying
fibrogenic
CLD
has
dramatically
improved,
boosting
pre-clinical
studies
clinical
trials
designed
to
find
novel
therapeutic
approaches.
From
these
several
critical
concepts
have
emerged,
starting
reveal
complexity
pro-fibrotic
microenvironment
which
involves
very
complex,
dynamic
interrelated
interactions
between
different
hepatic
extrahepatic
cell
populations.
This
review
will
offer
first
recapitulation
established
pathophysiological
basic
principles
by
intentionally
focus
attention
NAFLD/NASH,
metabolic-related
form
with
high
impact
general
population
emerging
leading
cause
worldwide.
NAFLD/NASH-related
pro-inflammatory
profibrogenic
be
analysed
information
cells,
mediators
signalling
pathways
taken
advantage
methodological
approaches
techniques
(single
genomics,
imaging
mass
cytometry,
vitro
two-
three-dimensional
models,
etc.).
We
next
overview
recent
advancement
diagnostic
prognostic
tools,
including
serum
biomarkers
polygenic
scores,
support
analysis
biopsies.
Finally,
this
provide
current
therapies
treatment
NAFLD/NASH
patients.
Science Translational Medicine,
Год журнала:
2023,
Номер
15(716)
Опубликована: Окт. 4, 2023
Metabolic
dysfunction–associated
steatohepatitis
(MASH)
is
a
severe
form
of
liver
disease
that
poses
global
health
threat
because
its
potential
to
progress
advanced
fibrosis,
leading
cirrhosis
and
cancer.
Recent
advances
in
single-cell
methodologies,
refined
models,
genetic
epigenetic
insights
have
provided
nuanced
understanding
MASH
fibrogenesis,
with
substantial
cellular
heterogeneity
livers
providing
potentially
targetable
cell-cell
interactions
behavior.
Unlike
mechanisms
underlying
fibrosis
regression
are
still
inadequately
understood,
although
antifibrotic
targets
been
recently
identified.
A
treatment
framework
could
lead
noninvasive
assessment
targeted
therapies
preserve
hepatocellular
function
restore
the
liver’s
architectural
integrity.
