Otology & Neurotology,
Journal Year:
2024,
Volume and Issue:
45(8), P. 947 - 953
Published: July 29, 2024
Gentamicin
is
a
commonly
used
aminoglycoside
antibiotic,
with
ototoxicity
as
significant
side
effect.
Ferroptosis,
an
iron-dependent
form
of
cell
death,
has
been
implicated
in
variety
disorders.
Whether
ferroptosis
impacts
gentamicin
not
yet
known.
The
current
work
in-vitro
model
to
examine
the
influence
gentamicin-induced
on
cochlear
hair
damage
and
probable
molecular
biological
pathways.
Frontiers in Immunology,
Journal Year:
2025,
Volume and Issue:
16
Published: Feb. 28, 2025
Diabetic
kidney
disease
(DKD)
is
a
prevalent
complication
of
diabetes
mellitus
(DM),
and
its
incidence
increasing
alongside
the
number
cases.
Effective
treatment
long-term
management
DKD
present
significant
challenges;
thus,
deeper
understanding
pathogenesis
essential
to
address
this
issue.
Chronic
inflammation
abnormal
cell
death
in
closely
associate
with
development.
Recently,
there
has
been
considerable
attention
focused
on
immune
infiltration
into
renal
tissues
inflammatory
response’s
role
progression.
Concurrently,
ferroptosis—a
novel
form
death—has
emerged
as
critical
factor
pathogenesis,
leading
increased
glomerular
filtration
permeability,
proteinuria,
tubular
injury,
interstitial
fibrosis,
other
pathological
processes.
The
cardiorenal
benefits
SGLT2
inhibitors
(SGLT2-i)
patients
have
demonstrated
through
numerous
large
clinical
trials.
Moreover,
further
exploratory
experiments
indicate
these
drugs
may
ameliorate
serum
urinary
markers
inflammation,
such
TNF-α,
inhibit
ferroptosis
models.
Consequently,
investigating
interplay
between
innate
responses
for
guiding
future
drug
This
review
presents
an
overview
within
context
DKD,
beginning
core
mechanisms
delving
potential
roles
We
will
also
analyze
how
aberrant
cells,
molecules,
signaling
pathways
contribute
Finally,
we
discuss
interactions
responses,
well
targeted
therapeutic
agents,
based
current
evidence.
By
analyzing
immunity
aim
provide
insights
development
area.
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(2), P. 196 - 196
Published: Feb. 4, 2024
Ferroptosis
is
an
iron-dependent
cell
death
pathway
that
involves
the
depletion
of
intracellular
glutathione
(GSH)
levels
and
iron-mediated
lipid
peroxidation.
experimentally
caused
by
inhibition
cystine/glutamate
antiporter
xCT,
which
depletes
cells
GSH,
or
peroxidase
4
(GPx4),
a
key
regulator
The
events
occur
between
GPx4
execution
ferroptotic
are
currently
matter
active
research.
Previous
work
has
shown
calcium
release
from
endoplasmic
reticulum
(ER)
mediated
ryanodine
receptor
(RyR)
channels
contributes
to
ferroptosis-induced
in
primary
hippocampal
neurons.
Here,
we
used
SH-SY5Y
neuroblastoma
cells,
do
not
express
RyR
channels,
test
if
inositol
1,4,5-trisphosphate
(IP3R)
channel
plays
role
this
process.
We
show
treatment
with
RAS
Selective
Lethal
Compound
3
(RSL3),
inhibitor,
enhanced
reactive
oxygen
species
(ROS)
generation,
increased
cytoplasmic
mitochondrial
levels,
peroxidation,
death.
RSL3-induced
signals
were
inhibited
Xestospongin
B,
specific
inhibitor
ER-resident
IP3R
channel,
decreasing
carbachol
IP3R1
knockdown,
also
prevented
changes
morphology
toward
roundness
induced
RSL3.
Intracellular
chelation
incubation
BAPTA-AM
signals,
affected
extracellular
depletion.
propose
activates
IP3R-mediated
leading
which,
turn,
stimulate
ROS
production
induce
peroxidation
noxious
positive
feedback
cycle.
Non-coding RNA Research,
Journal Year:
2024,
Volume and Issue:
9(4), P. 1159 - 1177
Published: May 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.
Cancer Cell International,
Journal Year:
2025,
Volume and Issue:
25(1)
Published: March 7, 2025
Ferroptosis
is
a
distinct
form
of
regulated
cell
death
characterized
by
iron-dependent
lipid
peroxidation,
playing
critical
role
in
various
diseases,
including
cancer,
neurodegeneration,
and
tissue
damage.
This
study
reviews
the
intricate
relationship
between
ferroptosis
Janus
kinase/signal
transducer
activator
transcription
(JAK/STAT)
signaling
pathway,
highlighting
its
regulatory
functions
across
multiple
biological
processes.
Dysregulation
JAK/STAT
pathway
implicated
promoting
or
inhibiting
ferroptosis,
depending
on
context.
JAK2
promotes
activating
STAT
proteins,
modulating
expression
key
regulators
like
SLC7A11
GPX4,
influencing
iron
homeostasis
through
pathways
such
as
ferritinophagy
hepcidin
regulation.
STAT1
activation
primarily
enhances
suppression
cystine-glutamate
antiporter
(System
Xc-),
leading
to
glutathione
depletion
contributing
conditions
Sjogren's
syndrome
age-related
macular
degeneration.
In
contrast,
STAT3
plays
protective
upregulating
which
inhibits
survival,
particularly
cancers
hepatocellular
carcinoma,
prostate
renal
carcinoma.
also
discusses
STAT6's
involvement
diseases
asthma
lung
injury
regulating
antioxidant
defenses.
Furthermore,
review
explores
potential
therapeutic
strategies
targeting
manipulate
for
disease
treatment.
cancer
therapy,
this
can
enhance
effectiveness
inducers,
offering
promising
avenues
overcome
drug
resistance.
Additionally,
interplay
immune
responses,
oxidative
stress,
metabolism
underscores
significance
progression
intervention.
By
exploring
these
mechanisms,
provides
insights
into
development
novel
treatments
modulation,
with
implications
inflammatory
neurodegenerative
conditions.
Bioconjugate Chemistry,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 5, 2025
Exogenous
iron
delivery
using
iron-containing
nanomaterials
is
an
alternative
strategy
for
enhancing
the
efficacy
in
ferroptosis
tumor
therapy
but
limited
by
problems
of
low
content,
enrichment,
cellular
uptake,
and
uncontrolled
release
ions.
To
solve
problems,
FeOOH-assisted
approach
demonstrated
to
produce
hybrid
polymer
nanospindles
(IHPNSs)
efficient
therapy.
The
IHPNSs
are
prepared
through
cohydrolysis
FeCl3·6H2O
with
aniline,
pyrrole,
or
amino-pyrrole.
On
one
hand,
hydrolysis
Fe3+
generates
FeOOH
particles,
which
further
act
as
templates
form
fusiform
architectures.
other
triggers
oxidative
polymerization
as-prepared
polymers
capable
coordinating
excessive
locate
on
templates,
thus
producing
Fe3+/polymer
composite-coated
nanospindles.
Systematic
studies
indicate
that
one-dimension-like
morphology
facilitates
enrichment
uptake
IHPNSs.
Besides
high
content
IHPNSs,
controlled
stimulated
overexpressed
glutathione
(GSH)
microenvironment
achieved.
released
transformed
Fe2+
scavenging
GSH,
leads
accumulation
reactive
oxygen
species
lipid
peroxides
finally
induces
cells.
As
a
proof
concept,
show
good
treatment
rat
model
bladder
tumors
situ.
