Oncology Letters,
Journal Year:
2024,
Volume and Issue:
28(6)
Published: Oct. 14, 2024
Cholangiocarcinoma
(CCA)
is
a
malignant
tumor
that
arises
within
the
biliary
system,
which
exhibits
progressively
increasing
incidence
and
poor
patient
prognosis.
A
thorough
understanding
of
molecular
pathogenesis
drives
progression
CCA
essential
for
development
effective
target
therapeutic
approaches.
Ferroptosis
driven
by
excessive
iron
accumulation
catalysis,
lipid
peroxidation
failure
antioxidant
defense
systems.
Key
targets
metabolism,
metabolism
systems
involve
molecules
such
as
transferrin
receptor,
ACSL4
GPX4,
respectively.
Inhibitors
ferroptosis
include
ferrostatin-1,
liproxstatin-1,
vitamin
E
coenzyme
Q10.
By
contrast,
compounds
erastin,
RSL3
FIN56
have
been
identified
inducers
ferroptosis.
serves
notable
role
in
onset
CCA.
cells
exhibit
high
sensitivity
to
aberrant
these
increases
oxidative
stress
accumulation.
The
induction
markedly
reduces
ability
proliferate
migrate.
Certain
agonists,
cause
peroxide
build
up
GPX4
inhibition
induce
cells.
Current
serological
markers,
CA-199,
low
specificity
difficulties
diagnosis
However,
novel
techniques,
non-invasive
liquid
biopsy
assays
markers
double-cortin-like
kinase
1,
could
improve
diagnostic
accuracy.
primarily
treated
with
surgery
chemotherapy.
close
association
between
mechanisms
related
regulatory
pathways
has
demonstrated.
Therefore,
it
be
suggested
multi-targeted
approaches,
inducers,
chelating
agents
modulators
YL-939,
may
treatment
efficacy.
Iron
death-related
genes,
are
highly
expressed
associated
prognosis
patients
represent
potential
prognostic
present
review
focused
on
p53
ACSL4,
process
targeted
medications
combination
PDT
peroxidation,
Xc
Aging-related
disorders
pose
significant
challenges
due
to
their
complex
interplay
of
physiological
and
metabolic
factors,
including
inflammation,
oxidative
stress,
mitochondrial
dysfunction.
Curcumin,
a
natural
compound
with
potent
antioxidant
anti-inflammatory
properties,
has
emerged
as
promising
candidate
for
mitigating
these
age-related
processes.
However,
gaps
in
understanding
the
precise
mechanisms
curcumin's
effects
optimal
dosages
different
conditions
necessitate
further
investigation.
This
systematic
review
synthesizes
current
evidence
on
potential
addressing
disorders,
emphasizing
its
impact
cognitive
function,
neurodegeneration,
muscle
health
older
adults.
By
evaluating
safety,
efficacy,
action
curcumin
supplementation,
this
aims
provide
insights
into
therapeutic
promoting
healthy
aging.
A
search
across
three
databases
using
specific
keywords
yielded
2,256
documents,
leading
selection
15
clinical
trials
synthesis.
Here
we
highlight
multifaceted
agent
combating
disorders.
The
findings
suggest
that
could
offer
effective
approach
enhancing
quality
life
aging
individuals.
Further
research
well-designed
are
essential
validate
optimize
use
personalized
medicine
approaches
conditions.
Nutrients,
Journal Year:
2024,
Volume and Issue:
16(16), P. 2721 - 2721
Published: Aug. 15, 2024
Aging-related
disorders
pose
significant
challenges
due
to
their
complex
interplay
of
physiological
and
metabolic
factors,
including
inflammation,
oxidative
stress,
mitochondrial
dysfunction.
Curcumin,
a
natural
compound
with
potent
antioxidant
anti-inflammatory
properties,
has
emerged
as
promising
candidate
for
mitigating
these
age-related
processes.
However,
gaps
in
understanding
the
precise
mechanisms
curcumin’s
effects
optimal
dosages
different
conditions
necessitate
further
investigation.
This
systematic
review
synthesizes
current
evidence
on
potential
addressing
disorders,
emphasizing
its
impact
cognitive
function,
neurodegeneration,
muscle
health
older
adults.
By
evaluating
safety,
efficacy,
action
curcumin
supplementation,
this
aims
provide
insights
into
therapeutic
promoting
healthy
aging.
A
search
across
three
databases
using
specific
keywords
yielded
2256
documents,
leading
selection
15
clinical
trials
synthesis.
Here,
we
highlight
multifaceted
agent
combating
disorders.
The
findings
suggest
that
could
offer
effective
approach
enhancing
quality
life
aging
individuals.
Further
research
well-designed
are
essential
validate
optimize
use
personalized
medicine
approaches
conditions.
Journal of Neuroinflammation,
Journal Year:
2025,
Volume and Issue:
22(1)
Published: Feb. 7, 2025
Mitochondrial
dysfunction
is
a
pivotal
instigator
of
neuroinflammation,
with
mitochondrial
DNA
(mtDNA)
leakage
as
critical
intermediary.
This
review
delineates
the
intricate
pathways
leading
to
mtDNA
release,
which
include
membrane
permeabilization,
vesicular
trafficking,
disruption
homeostatic
regulation,
and
abnormalities
in
dynamics.
The
escaped
activates
cytosolic
sensors,
especially
cyclic
gmp-amp
synthase
(cGAS)
signalling
inflammasome,
initiating
neuroinflammatory
cascades
via
pathways,
exacerbating
spectrum
neurological
pathologies.
therapeutic
promise
targeting
discussed
detail,
underscoring
necessity
for
multifaceted
strategy
that
encompasses
preservation
homeostasis,
prevention
leakage,
reestablishment
dynamics,
inhibition
activation
sensors.
Advancing
our
understanding
complex
interplay
between
neuroinflammation
imperative
developing
precision
interventions
disorders.
Journal of Inflammation Research,
Journal Year:
2024,
Volume and Issue:
Volume 17, P. 7819 - 7835
Published: Oct. 1, 2024
Sepsis
is
a
common
critical
illness
characterized
by
high
mortality
rates
and
significant
disease
burden.
In
the
context
of
sepsis-induced
organ
dysfunction,
lungs
are
among
initial
organs
affected,
which
may
progress
to
acute
lung
injury
(ALI)
respiratory
distress
syndrome
(ARDS).
Recent
studies
have
highlighted
crucial
roles
mitophagy
ferroptosis
in
development
progression
ALI/ARDS.
Identifying
key
convergence
points
these
processes
provide
valuable
insights
for
treatment
this
condition.
recent
years,
certain
herbs
their
bioactive
compounds
demonstrated
unique
benefits
managing
ALI/ARDS
modulating
or
ferroptosis.
This
review
summary
mechanisms
ferroptosis,
explores
interactions,
emphasizes
regulatory
Additionally,
it
offers
novel
perspective
on
strategies
summarizing
various
relevant
Metabolites,
Journal Year:
2025,
Volume and Issue:
15(2), P. 93 - 93
Published: Feb. 3, 2025
Background:
Alzheimer’s
disease
is
a
central
nervous
system
degenerative
closely
related
to
age
with
complex
pathogenesis.
As
natural
medicinal
plant,
forest-grown
ginseng
(GSF)
contains
abundant
ginsenosides
and
offers
significant
neuroprotective
effects.
Methods:
In
this
study,
we
comprehensively
investigated
the
effect
of
GSF
on
cell
viability
PC12
cells
in
an
AD
model
alongside
metabolic
changes
serum
brains
mice,
combined
efficacy
evaluation
vitro
UHPLC-MS-based
metabolomics
vivo.
The
goal
study
clarify
potential
mechanism
treating
AD.
Results:
results
showed
that
can
promote
proliferation
cells,
reduce
content
IL-8,
increase
activity
SOD,
alleviate
inflammation
oxidative
stress
induced
by
Aβ25~35.
immunohistochemical
for
mouse
brain
tissue
also
could
inflammatory
response
reducing
overexpression
IBa1.
was
alleviated
Aβ
protein
deposition
tissue.
An
untargeted
analysis
performed
using
UHPLC-Q-Exactive
MS
principal
component
(PCA)
identify
differentially
expressed
metabolites
mice
after
treatment.
Twenty
seventeen
different
were
identified
tissue,
respectively.
pathway
enrichment
differential
treat
up-regulating
succinic
acid
semialdehyde,
carbamoyl
phosphate,
Sphingosine
1-phosphate,
L-cystathionine,
2-ketobutyric
acid,
Vanillylmandelic
D-Ribose
regulate
sphingomyelin
metabolism,
synthesis
metabolism
neurotransmitters
precursors,
energy
metabolism.
Conclusions:
neuroinflammation
regulating
disorders
amino
acids,
sphingolipids,
unsaturated
fatty
arachidonic
metabolites.
These
suggest
link
between
metabolite
imbalance
AD,
reveal
basis
BMC Gastroenterology,
Journal Year:
2025,
Volume and Issue:
25(1)
Published: Feb. 5, 2025
Severe
acute
pancreatitis
(SAP)
has
high
morbidity,
a
complicated
and
dangerous
course,
many
complications,
including
severe
pulmonary
complications.
SAP-associated
lung
injury
(SAP-ALI)
is
still
significant
challenge
for
surgeons
because
of
its
mortality.
Therefore,
more
effective
treatment
methods
are
urgently
needed.
Emodin
(EMO)
shown
tremendous
potential
in
treating
refractory
diseases.
However,
protection
mechanism
SAP-ALI
needs
to
be
further
clarified.
This
study
was
undertaken
investigate
the
protective
effects
EMO
against
SAP
rats
alveolar
epithelial
cells,
with
particular
focus
on
classical
ferroptosis
pathway.
In
an
vivo
study,
forty
SD
were
evenly
split
into
five
groups:
sham
operation
(SO)
group,
biliopancreatic
duct
retrogradely
injected
5%
sodium
taurocholate
(STC)
create
+
group
administered
via
gavage
following
modeling,
ML385
(a
given
inhibitor
nuclear
factor
erythroid
2-related
2
(Nrf2)),
group.
vitro
A549
cell
lines
exposed
lipopolysaccharide
(LPS)
treated
EMO.
also
used
inhibit
expression
Nrf2.
Pancreatic
tissue
damage
evaluated
using
histological
examination
molecular
experiments.
Enzyme-linked
immunosorbent
assays
(ELISA)
assess
levels
pro-inflammatory
cytokines,
Fe2+,
associated
oxidative
stress
indicators
serum
supernatant.
Real-time
polymerase
chain
reaction
(PCR),
Western
blot
(WB),
immunofluorescence
find
expressions
related
mRNAs
proteins
or
cells.
The
findings
demonstrated
that
suppressing
Nrf2
exacerbated
inflammatory
response
brought
by
pathological
alterations
SAP-ALI.
reversed
this
change
activating
Nrf2/Heme
Oxygenase-1
(HO-1)/glutathione
peroxidase
4
(GPX4)
signal
path.
Moreover,
these
results
showed
EMO,
contrary
ML385,
suppressed
response,
which
manifested
as
up-regulated
glutathione
(GSH)
GPX4
down-regulated
malondialdehyde
(MDA),
superoxide
dismutase
(SOD),
reactive
oxygen
species
(ROS)
levels.
Our
effectively
inhibited
both
vitro,
while
modulating
Nrf2/HO-1/GPX4
signaling
pathway
provide