Frontiers in Immunology,
Год журнала:
2024,
Номер
15
Опубликована: Дек. 12, 2024
Ferroptosis
is
a
novel
form
of
cell
death
characterized
by
unlimited
accumulation
iron-dependent
lipid
peroxides.
It
often
accompanied
disease,
and
the
relationship
between
ferroptosis
immune
cells
regulation
has
been
attracting
increasing
attention.
Initially,
it
was
found
in
cancer
research
that
inhibition
regulatory
T
(Treg)
promotion
CD8+
jointly
promoted
formation
an
immune-tolerant
environment
tumors.
T-cell
subsequently
to
have
immunoregulatory
effects
other
diseases.
As
autoimmune
disease
imbalance,
attracted
attention
for
its
potential
regulating
balance
lupus
nephritis.
This
article
reviews
metabolic
processes
within
different
subsets
nephritis
(LN),
including
follicular
helper
(TFH)
cells,
(Th)17
Th1
Th2
Treg
reveals
these
cellular
metabolisms
not
only
facilitate
imbalance
but
are
also
closely
associated
with
occurrence
ferroptosis.
Consequently,
we
hypothesize
targeting
pathways
could
become
direction
effectively
treating
altering
differentiation
incidence
Frontiers in Oncology,
Год журнала:
2024,
Номер
14
Опубликована: Авг. 12, 2024
Ferroptosis
is
an
iron-dependent
form
of
cell
death
that
results
from
excess
lipid
peroxidation
in
cellular
membranes.
Within
the
last
decade,
physiological
and
pathological
roles
for
ferroptosis
have
been
uncovered
autoimmune
diseases,
inflammatory
conditions,
infection,
cancer
biology.
Excitingly,
metabolism
may
be
targeted
to
induce
by
cancers
are
resistant
other
forms
death.
sensitivity
regulated
oxidative
stress,
metabolism,
iron
which
all
influenced
tumor
microenvironment
(TME).
Whereas
some
types
shown
adapt
these
stressors,
it
not
clear
how
immune
cells
regulate
their
sensitivities
ferroptosis.
In
this
review,
we
discuss
mechanisms
different
subsets,
influences
infiltrate
TME,
interactions
can
determine
epithelial-to-mesenchymal
transition
(EMT)
metastasis.
While
much
focus
has
placed
on
inducing
cells,
important
considerations
ferroptosis-modulating
strategies
impact
anti-tumor
immunity.
From
perspective,
also
promising
immunotherapies
field
challenges
associated
with
targeting
specific
populations.
Non-coding RNA Research,
Год журнала:
2024,
Номер
9(4), С. 1159 - 1177
Опубликована: Май 20, 2024
Ferroptosis,
a
recently
identified
type
of
non-apoptotic
cell
death,
triggers
the
elimination
cells
in
presence
lipid
peroxidation
and
an
iron-dependent
manner.
Indeed,
ferroptosis-stimulating
factors
have
ability
suppressing
antioxidant
capacity,
leading
to
accumulation
reactive
oxygen
species
(ROS)
subsequent
oxidative
death
cells.
Ferroptosis
is
involved
pathophysiological
basis
different
maladies,
such
as
multiple
cancers,
among
which
female-oriented
malignancies
attracted
much
attention
recent
years.
In
this
context,
it
has
also
been
unveiled
that
non-coding
RNA
transcripts,
including
microRNAs,
long
RNAs,
circular
RNAs
regulatory
interconnections
with
ferroptotic
flux,
controls
pathogenic
development
diseases.
Furthermore,
potential
employing
these
transcripts
therapeutic
targets
during
onset
female-specific
neoplasms
modulate
ferroptosis
become
research
hotspot;
however,
molecular
mechanisms
functional
alterations
still
require
further
investigation.
The
current
review
comprehensively
highlights
its
association
focus
on
how
crosstalk
affects
pathogenesis
malignancies,
from
breast
cancer
ovarian,
cervical,
endometrial
neoplasms,
suggesting
novel
decelerate
even
block
expansion
tumors.
ACS Catalysis,
Год журнала:
2025,
Номер
unknown, С. 3570 - 3583
Опубликована: Фев. 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.
Frontiers in Immunology,
Год журнала:
2025,
Номер
16
Опубликована: Март 11, 2025
Ferroptosis,
an
iron-dependent
form
of
regulated
cell
death
driven
by
lipid
peroxidation,
plays
a
pivotal
role
in
various
physiological
and
pathological
processes.
In
this
review,
we
summarize
the
core
mechanisms
ferroptosis,
emphasizing
its
intricate
connections
to
metabolism,
including
fatty
acid
synthesis,
phospholipid
remodeling,
oxidation
dynamics.
We
further
highlight
advancements
detection
technologies,
such
as
fluorescence
imaging,
lipidomics,
vivo
PET
which
have
deepened
our
understanding
ferroptotic
regulation.
Additionally,
discuss
ferroptosis
human
diseases,
where
it
acts
double-edged
sword,
contributing
cancer
while
also
driving
ischemia-reperfusion
injury
neurodegeneration.
Finally,
explore
therapeutic
strategies
aimed
at
either
inducing
or
inhibiting
iron
chelation,
antioxidant
modulation,
lipid-targeted
interventions.
By
integrating
mechanistic
insights,
disease
relevance,
potential,
review
provides
comprehensive
perspective
on
crucial
interface
between
metabolism
oxidative
stress.
Biochemical Pharmacology,
Год журнала:
2025,
Номер
unknown, С. 116907 - 116907
Опубликована: Март 1, 2025
Ischemic
stroke
is
a
debilitating
condition
characterized
by
high
morbidity,
disability,
recurrence,
and
mortality
rates
on
global
scale,
posing
significant
threat
to
public
health
economic
stability.
Extensive
research
has
thoroughly
explored
the
molecular
mechanisms
underlying
ischemic
stroke,
elucidating
strong
association
between
soluble
N-ethylmaleimide-sensitive
factor
(NSF)
attachment
protein
receptor
proteins
(SNAREs)
pathogenesis
of
this
condition.
SNAREs,
class
highly
conserved
involved
in
membrane
fusion,
play
crucial
role
modulating
neuronal
information
transmission
promoting
myelin
formation
central
nervous
system
(CNS).
Preventing
SNARE
complex
formation,
malfunctions
SNARE-dependent
exocytosis,
altered
regulation
SNARE-mediated
vesicle
fusion
are
linked
excitotoxicity,
endoplasmic
reticulum
(ER)
stress,
programmed
cell
death
(PCD)
stroke.
However,
its
remain
unclear.
This
study
conducts
comprehensive
review
existing
literature
proteins,
encompassing
structure,
classification,
expression
family,
as
well
assembly
-
disassembly
cycle
complexes
their
physiological
roles
CNS.
We
examine
which
SNAREs
contribute
pathological
progression
associated
risk
factors
(hypertension,
hyperglycemia,
dyslipidemia,
atherosclerosis).
Furthermore,
our
findings
highlight
promise
viable
target
for
pharmacological
interventions
treatment
