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
Cardiovascular Diabetology,
Год журнала:
2024,
Номер
23(1)
Опубликована: Март 19, 2024
Abstract
The
9th
Cardiovascular
Outcome
Trial
(CVOT)
Summit:
Congress
on
Cardiovascular,
Kidney,
and
Metabolic
Outcomes
was
held
virtually
November
30-December
1,
2023.
This
reference
congress
served
as
a
platform
for
in-depth
discussions
exchange
recently
completed
outcomes
trials
including
dapagliflozin
(DAPA-MI),
semaglutide
(SELECT
STEP-HFpEF)
bempedoic
acid
(CLEAR
Outcomes),
the
advances
they
represent
in
reducing
risk
of
major
adverse
cardiovascular
events
(MACE),
improving
metabolic
outcomes,
treating
obesity-related
heart
failure
with
preserved
ejection
fraction
(HFpEF).
A
broad
audience
endocrinologists,
diabetologists,
cardiologists,
nephrologists
primary
care
physicians
participated
online
guideline
updates
management
disease
(CVD)
diabetes,
(HF)
chronic
kidney
(CKD);
type
1
diabetes
(T1D)
its
comorbidities;
CKD
SGLT2
inhibitors
non-steroidal
mineralocorticoid
receptor
antagonists
(nsMRAs);
treatment
obesity
GLP-1
dual
GIP/GLP-1
agonists.
association
nonalcoholic
steatohepatitis
(NASH;
dysfunction-associated
steatohepatitis,
MASH)
cancer
possible
treatments
these
complications
were
also
explored.
It
is
generally
assumed
that
diseases
equally
effective
all
patients.
However,
discussed
at
Summit,
this
assumption
may
not
be
true.
Therefore,
it
important
to
enroll
patients
from
diverse
racial
ethnic
groups
clinical
analyze
patient-reported
assess
efficacy,
develop
innovative
approaches
tailor
medications
those
who
benefit
most
minimal
side
effects.
Other
keys
successful
comorbidities,
dementia,
entail
use
continuous
glucose
monitoring
(CGM)
technology
implementation
appropriate
patient-physician
communication
strategies.
10th
Summit
will
December
5–6,
2024
(
http://www.cvot.org
).
Life,
Год журнала:
2024,
Номер
14(2), С. 272 - 272
Опубликована: Фев. 18, 2024
The
bidirectional
relationship
between
type
2
diabetes
and
(non-alcoholic
fatty
liver
disease)
NAFLD
is
indicated
by
the
higher
prevalence
worse
disease
course
of
one
condition
in
presence
other,
but
also
apparent
beneficial
effects
observed
one,
when
other
improved.
This
partly
explained
their
belonging
to
a
multisystemic
that
includes
components
metabolic
syndrome
shared
pathogenetic
mechanisms.
Throughout
progression
more
advanced
stages,
complex
systemic
local
derangements
are
involved.
During
fibrogenesis,
significant
reprogramming
occurs
hepatic
stellate
cells,
hepatocytes,
immune
engaging
carbohydrate
lipid
pathways
support
high-energy-requiring
processes.
natural
history
evolves
variable
dynamic
manner,
probably
due
interaction
number
modifiable
(diet,
physical
exercise,
microbiota
composition,
etc.)
non-modifiable
(genetics,
age,
ethnicity,
risk
factors
may
intervene
concomitantly,
or
subsequently/intermittently
time.
influence
(and
rate)
fibrosis
progression/regression.
recognition
control
determine
rapid
(or
its
regression)
critical,
as
stages
associated
with
liver-related
all-cause
mortality.
DNA and Cell Biology,
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 8, 2025
Liver
fibrosis,
one
of
the
main
histological
determinants
various
chronic
liver
diseases,
currently
lacks
effective
treatment.
Hepatic
stellate
cells
(HSCs)
are
pivotal
in
production
extracellular
matrix
and
amplify
fibrogenic
response.
Inhibiting
activation
HSCs
or
promoting
senescence
activated
is
crucial
for
regression
fibrosis.
The
ATPase
p97,
also
known
as
valosin-containing
protein
(VCP),
a
central
component
ubiquitin-proteasome
system,
it
regulates
numerous
cellular
processes
by
influencing
homeostasis.
In
this
study,
we
observed
an
upregulation
p97
expression
around
regions
exhibiting
fibrosis
diet-
chemical-induced
nonalcoholic
steatohepatitis
murine
model.
Intervention
with
antagonist
CB-5083
knockdown
reduced
alpha-smooth
muscle
actin
collagen-I
both
mouse
human
HSCs.
administration
induced
HSC
resulted
markers,
including
p21,
p53,
GPX4,
senescence-associated
β-galactosidase.
Furthermore,
treatment
inhibited
Yes-associated
(YAP),
which
senescence-related
regulatory
has
profibrotic
function.
We
used
to
treat
fibrotic
mice
found
that
was
inhibited,
attenuated.
addition,
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
