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
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: June 27, 2024
Ferroptosis,
a
new
type
of
programmed
cell
death
proposed
in
recent
years,
is
characterized
mainly
by
reactive
oxygen
species
and
iron-mediated
lipid
peroxidation
differs
from
death,
such
as
apoptosis,
necrosis,
autophagy.
Ferroptosis
associated
with
variety
physiological
pathophysiological
processes.
Recent
studies
have
shown
that
ferroptosis
can
aggravate
or
reduce
the
occurrence
development
diseases
targeting
metabolic
pathways
signaling
tumors,
ischemic
organ
damage,
other
degenerative
related
to
peroxidation.
Increasing
evidence
suggests
closely
linked
onset
progression
various
ophthalmic
conditions,
including
corneal
injury,
glaucoma,
age-related
macular
degeneration,
diabetic
retinopathy,
retinal
detachment,
retinoblastoma.
Our
review
current
research
on
reveals
significant
advancements
our
understanding
pathogenesis,
aetiology,
treatment
these
conditions.
ACS Catalysis,
Journal Year:
2025,
Volume and Issue:
unknown, P. 3570 - 3583
Published: Feb. 13, 2025
Human
ferroptosis
suppressor
protein
1
(HsFSP1)
is
an
NAD(P)H:quinone
oxidoreductase
with
broad
substrate
specificity
that
has
been
widely
implicated
in
aiding
malignant
neoplastic
cell
survival.
FSP1
myristoylated
and
associated
membranes,
where
it
regenerates
the
reduced
forms
of
quinones
using
electrons
from
NADPH.
The
quinol
products
intercept
reactive
oxygen
species
ameliorate
lipid
peroxidation,
preventing
ferroptosis,
a
form
regulated
death.
While
enzymes
have
reported
to
6-OH-FAD
as
active
cofactor,
aerobic
titration
enzyme
NADPH
presence
absence
ubiquinone
(UQ)
reveals
this
more
likely
artifact
native
HsFSP1
unmodified
FAD
cofactor.
Moreover,
suppresses
reaction
molecular
three-fold
which,
kinetic
standpoint,
severely
limits
opportunity
for
cofactor
modification.
isolated
NADP+
bound
rate
release
product
observed
reduction
by
NAD(P)H
molecules.
occurs
rapidly
(≥2000
s–1),
dictating
turnover
wholly
defined
HsFSP1·NADP+
complex.
Given
does
not
distinguish
ubiquinol
significant
differences
binding
affinity,
pronounced
catalytic
commitment
quinone
serves
overcome
presumed
limitations
imposed
abundance
relative
membrane.
This
characteristic
also
maintains
ostensibly
fully
oxidized
state
under
conditions,
futile
dioxygen.
Brain Injury,
Journal Year:
2025,
Volume and Issue:
unknown, P. 1 - 11
Published: April 16, 2025
Cells
universally
employ
an
efficiency-driven
metabolic
switch
mechanism
during
nutritional
changes,
growth,
and
differentiation,
transitioning
from
oxidative
phosphorylation
(OXPHOS)
to
glycolysis
ensure
survival
under
hypoxic
conditions
or
high
energy
demands.
In
cerebral
ischemia,
inadequate
blood
supply
causes
oxygen
deprivation,
prompting
brain
cells
initiate
glycolytic
reprogramming
meet
urgent
needs.
While
this
adaptation
is
a
temporary
solution,
it
may
lead
lactic
acidosis,
aggravated
inflammation,
increased
free
radical
production.
Prolonged
reperfusion
with
sustained
can
exacerbate
cell
damage,
potentially
causing
irreversible
harm.
This
review
systematically
examines
the
dynamic
changes
in
glucose
transport
mechanisms
roles
of
immediate,
early,
intermediate,
late
responder
cells,
along
their
regulatory
factors,
reprogramming.
Using
temporal
analysis
framework
based
on
body's
natural
response
sequence
pathological
events,
we
elucidate
how
at
different
stages
collaborate
address
metabolism
conditions.
Reversing
inhibiting
improve
processes
ischemic
stroke,
offering
potential
therapeutic
benefits.
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(7), P. 820 - 820
Published: July 8, 2024
Dietary
restriction
(DR)
protocols
frequently
employ
intermittent
fasting.
Following
a
period
of
fasting,
meal
consumption
increases
lipogenic
gene
expression,
including
that
NADPH-generating
enzymes
fuel
lipogenesis
in
white
adipose
tissue
(WAT)
through
the
induction
transcriptional
regulators
SREBP-1c
and
CHREBP.
knockout
mice,
unlike
controls,
did
not
show
an
extended
lifespan
on
DR
diet.
WAT
cytoplasmic
NADPH
is
generated
by
both
malic
enzyme
1
(ME1)
pentose
phosphate
pathway
(PPP),
while
liver
primarily
synthesized
folate
cycle
provided
one-carbon
units
serine
catabolism.
During
daily
fasting
diet,
fatty
acids
are
released
from
transported
to
peripheral
tissues,
where
they
used
for
beta-oxidation
phospholipid
lipid
droplet
synthesis,
monounsaturated
(MUFAs)
may
activate
Nrf1
inhibit
ferroptosis
promote
longevity.
Decreased
PPP
stimulated
browning
protected
high-fat
high
levels
macrophages
linked
obesity.
But
oscillations
[NADPH]/[NADP+]
feeding
cycles
play
important
role
maintaining
metabolic
plasticity
drive
Studies
measuring
malate/pyruvate
as
proxy
[NADPH]/[NADP+],
well
studies
using
fluorescent
biosensors
expressed
animal
models
monitor
changes
needed
during
ad
libitum
diets
determine
associated
with
