Molecular Medicine,
Journal Year:
2024,
Volume and Issue:
30(1)
Published: Dec. 19, 2024
Acetaminophen
(APAP)-induced
acute
liver
injury
(AILI)
is
the
most
prevalent
cause
of
failure
and
mitochondrial
dysfunction
plays
a
dominant
role
in
pathogenesis
AILI.
Mitochondrial
transcription
factor
A
(TFAM)
an
important
marker
for
maintaining
functional
homeostasis,
but
its
functions
AILI
are
unclear.
This
study
aimed
to
investigate
function
TFAM
regulatory
molecular
mechanism
progression
Cardiorenal Medicine,
Journal Year:
2025,
Volume and Issue:
unknown, P. 1 - 21
Published: Jan. 21, 2025
Introduction:
The
objective
of
this
research
is
to
explore
the
possible
link
between
markers
liver
fibrosis
and
survival
rates
in
a
group
adults
who
have
been
diagnosed
with
both
chronic
kidney
disease
(CKD)
coronary
artery
(CAD).
Methods:
National
Health
Nutrition
Examination
Survey
(NHANES)
data
(1999-2018)
for
participants
CAD
CKD
were
analyzed.
Fibrosis-4
Index
(FIB-4),
Nonalcoholic
Fatty
Liver
Score
(NFS),
Forns
index
Aspartate
Aminotransferase/Alanine
Aminotransferase
(AST/ALT)
ratio
identified
as
crucial
biomarkers.
All-cause
cardiovascular
(CVD)
mortality
primary
outcomes,
assessed
using
Cox
models,
Kaplan-Meier
curves,
ROC
analysis.
Results:
A
total
1,192
patients
included.
regression
analysis
revealed
substantial
correlations
elevated
FIB-4,
NFS,
AST/ALT
levels
heightened
risk
all-cause
(HR
1.188,
95%CI
1.108-1.274;
HR
1.145,
1.069-1.227;
1.142,
1.081-1.201;
1.316,
1.056-1.639,
respectively)
CVD
1.133,
1.007-1.275;
1.155,
1.024-1.303;
1.208,
1.109-1.316
1.636,
1.203-2.224,
respectively).
indicated
comparable
predictive
accuracy
all
three
biomarkers,
showing
slightly
superior
performance.
Conclusion:
markers,
including
AST/ALT,
are
significant
predictors
CAD-CKD
patients.
ratio,
being
easily
measurable,
may
serve
an
effective
tool
stratification
population.
Frontiers in Pharmacology,
Journal Year:
2025,
Volume and Issue:
16
Published: Feb. 3, 2025
Background
and
purpose
2,3,5,4′-tetrahydroxystilbene-2-O-β-D-glucoside
(TSG)
exhibits
a
dualistic
pharmacological
profile,
acting
as
both
hepatoprotective
hepatotoxic
agent,
which
is
intricately
linked
to
its
interaction
with
multiple
signaling
pathways
stereoisomeric
forms,
namely,
cis-SG
trans-SG.
The
of
this
study
evaluate
the
effects
TSG
give
therapeutic
guidance.
Methods
This
performed
systematic
search
eight
databases
identify
preclinical
literature
up
until
March
2024.
CAMARADES
system
evaluated
evidence
quality
bias.
STATA
Python
were
used
for
statistical
analysis,
including
dose-effect
maps,
3D
maps
radar
charts
show
dose-time-effect
relationship
on
hepatoprotection
hepatotoxicity.
Results
After
rigorous
screening
process,
total
24
studies
encompassing
564
rodents
selected
inclusion
in
study.
findings
revealed
that
exhibited
bidirectional
levels
ALT
AST,
while
also
regulating
ALT,
TNF-α,
IL-6,
serum
TG,
TC,
SOD,
MDA,
IFN-γ,
apoptosis
rate.
histological
analysis
liver
tissue
confirmed
regulatory
TSG,
comprehensive
optimal
protective
dosage
range
was
27.27–38.81
mg/kg/d
toxic
51.93–76.07
mg/kg/d.
exerts
dual
injury
(LI)
through
network
Keap1/Nrf2/HO-1/NQO1,
NF-κB,
PPAR,
PI3K/Akt,
JAK/STAT
TGF-β
pathways.
Conclusion
could
mediate
oxidation,
inflammation,
metabolism
result
(27.27–38.81
mg/kg/d)
hepatotoxicity
(51.93–76.07
mg/kg/d).
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(4), P. 1493 - 1493
Published: Feb. 11, 2025
(1)
Liver
injury
caused
by
an
overdose
of
acetaminophen
(APAP)
represents
a
major
public
health
concern.
Paeoniflorin
(PF)
has
been
reported
to
have
anti-inflammatory
and
liver-protective
effects,
but
the
underlying
mechanisms
remain
unclear.
This
study
aimed
investigate
effect
PF
on
crosstalk
between
pyroptosis
NETs
in
AILI.
(2)
APAP-treated
C57BL/6J
mice
were
used
demonstrate
protective
liver
injury.
HepG2
dHL-60
cells
cultured
effects
hepatocyte
neutrophil
extracellular
traps
(NETs)
vitro.
Moreover,
cell
co-culture
experiments
performed,
treated
with
NETs-depleting
agent
inhibitor
improvement
AILI
induced
through
regulating
NETs.
(3)
significantly
alleviated
Additionally,
inhibited
expression
pyroptosis-related
proteins,
high-mobility
group
box
1
(HMGB1),
NETs-associated
proteins
vitro
vivo.
The
demonstrated
that
not
only
triggered
pyroptosis,
also
suppressed
In
depleted
neutrophils,
level
notably
decreased,
indicating
diminished
impact
PF.
Similarly,
formation
was
reduced
receiving
compared
APAP
group.
Compared
DNase
I
alone,
reduction
combined
serum
ALT
AST
levels
decreased
from
46.857%
39.927%
44.347%
33.419%,
respectively.
DSF
45.347%
36.419%,
(4)
therapeutic
Its
mechanism
involves
regulation
research
substantiates
pharmacological
promise
as
intervention
for
acute
The American Journal of Chinese Medicine,
Journal Year:
2025,
Volume and Issue:
unknown, P. 1 - 20
Published: March 27, 2025
Acetaminophen
(APAP)-induced
liver
injury
(AILI)
is
a
universal
disease
and
the
predominant
cause
of
acute
failure
in
clinical
practice.
Autophagy
highly
conserved
intracellular
degradation
pathway,
with
accumulating
evidence
indicating
its
involvement
APAP
hepatotoxicity.
Notably,
serine/threonine
AMP-activated
protein
kinase
(AMPK)/mammalian
target
rapamycin
(mTOR)/unc-51-like
1
(ULK1)
pathway
serves
as
most
classical
autophagy
engages
activation.
Thus,
pharmacological
activation
AMPK/mTOR/ULK1
has
emerged
critical
strategy
for
addressing
AILI.
Chlorogenic
acid
(CGA),
main
bioactive
constituent
isolated
from
Lonicera
japonica
Thunb.,
an
regulator
potential
AILI
therapy.
However,
whether
how
CGA
modulates
to
antagonize
not
yet
been
elucidated.
In
present
study,
we
aim
explore
impact
on
AILI,
well
underlying
mechanisms
vitro
vivo.
The
results
demonstrated
that
could
protect
mice
LO2
cells
oxidative
stress
induced
by
APAP.
Regarding
mechanisms,
activated
thereby
promoting
autophagy.
This
was
evidenced
p62/SQSTM1
(hereafter
referred
p62),
up-regulation
LC3B,
ATG5,
Beclin1.
It
worth
noting
aforementioned,
CGA-provided
beneficial
effects
were
abrogated
inhibition
AMPK
Compound
C
(CC,
inhibitor).
These
[Formula:
see
text]
alleviates
APAP,
which
contingent
upon
regulatory
effect
axis.
