Journal of Inflammation Research,
Journal Year:
2024,
Volume and Issue:
Volume 17, P. 10785 - 10805
Published: Dec. 1, 2024
Ulcerative
colitis
(UC),
a
major
type
of
inflammatory
bowel
disease,
is
characterized
by
chronic
inflammation
the
colonic
mucosa
and
submucosa.
Estrogen
receptor
β
(ERβ)
predominates
in
colon
exerts
anti-inflammatory
effects.
Ferroptosis,
recently
discovered
form
iron-dependent
programmed
cell
death,
implicated
pathogenesis
several
diseases,
including
UC.
However,
link
between
ferroptosis
actions
ERβ
UC
remains
to
be
elucidated.
Cell Death Discovery,
Journal Year:
2025,
Volume and Issue:
11(1)
Published: Jan. 29, 2025
Abstract
Lung
carcinoma
incidence
and
fatality
rates
remain
among
the
highest
on
a
global
scale.
The
efficacy
of
targeted
therapies
immunotherapies
is
commonly
compromised
by
emergence
drug
resistance
other
factors,
resulting
in
lack
durable
therapeutic
benefits.
Ferroptosis,
distinct
pattern
cell
death
marked
buildup
iron-dependent
lipid
peroxides,
has
been
shown
to
be
novel
potentially
more
effective
treatment
for
lung
carcinoma.
However,
mechanism
regulatory
network
ferroptosis
are
exceptionally
complex,
many
unanswered
questions
remain.
In
addition,
research
diagnosis
cancer
growing
exponentially.
Therefore,
it
necessary
provide
thorough
summary
latest
advancements
field
ferroptosis.
Here,
we
comprehensively
analyze
mechanisms
underlying
preconditions
ferroptosis,
defense
system,
associated
molecular
networks.
potential
strategies
also
highlighted.
Targeting
improves
tumor
enhances
effectiveness
drugs
immunotherapies.
These
findings
may
shed
fresh
light
management
carcinoma,
as
well
development
related
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(8), P. 4559 - 4559
Published: April 22, 2024
Oxidative
stress
and
lipid
peroxidation
play
important
roles
in
numerous
physiological
pathological
processes,
while
the
bioactive
products
of
peroxidation,
hydroperoxides
reactive
aldehydes,
act
as
mediators
redox
signaling
normal
malignant
cells.
Many
types
cancer,
including
osteosarcoma,
express
altered
pathways.
Such
pathways
protect
cancer
cells
from
cytotoxic
effects
oxidative
stress,
thus
supporting
transformation,
eventually
anticancer
therapies
associated
with
stress.
In
this
review,
we
aim
to
explore
status
osteosarcoma
highlight
involvement
pathways,
therapies.
Cancer Drug Resistance,
Journal Year:
2025,
Volume and Issue:
8(1)
Published: Jan. 6, 2025
Ferroptosis
is
an
iron-dependent
form
of
programmed
cell
death
induced
by
lipid
peroxidation.
This
process
regulated
signaling
pathways
associated
with
redox
balance,
iron
metabolism,
and
metabolism.
Cancer
cells'
increased
demand
makes
them
especially
susceptible
to
ferroptosis,
significantly
influencing
cancer
development,
therapeutic
response,
metastasis.
Recent
findings
indicate
that
cells
can
evade
ferroptosis
downregulating
key
related
this
process,
contributing
drug
resistance.
underscores
the
possibility
modulating
as
approach
counteract
resistance
enhance
efficacy.
review
outlines
involved
in
their
interactions
cancer-related
pathways.
We
also
highlight
current
understanding
resistance,
offering
insights
into
how
targeting
provide
novel
approaches
for
drug-resistant
cancers.
Finally,
we
explore
potential
ferroptosis-inducing
compounds
examine
challenges
opportunities
development
evolving
field.
Pharmacognosy Magazine,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 13, 2025
Background
Activation
of
PRR11
contributes
to
the
progression
lung
cancer
and
is
related
its
methylation
status.
However,
regulatory
mechanism
luteolin-zinc
(Lu-Zn)
on
methylation-mediated
under
hypoxic
conditions
remains
be
explored..
Purpose
This
study
aims
investigate
inhibitory
effect
Lu-Zn
cells,
regulation
ferroptosis,
role
in
hypoxia.
Methods
In
vitro
experiments
were
conducted
evaluate
focusing
impact
invasion,
migration,
ferroptosis.
The
expression
levels
PRR11,
status,
microRNA-6769b-3p
(miR-6769b-3p)
also
analyzed.
Results
Under
conditions,
significantly
inhibited
invasion
migration
abilities
cells
promoted
Additionally,
reversed
pro-cancer
effects
induced
by
PRR11.
At
molecular
level,
regulated
miR-6769b-3p.
Conclusion
Our
demonstrates
that
enhances
reduces
through
leads
inhibition
downstream
PI3K/AKT/mTOR
signaling
pathway,
promoting
ferroptosis
exerting
anti-lung
effects.
Journal of Biological Chemistry,
Journal Year:
2025,
Volume and Issue:
unknown, P. 108312 - 108312
Published: Feb. 1, 2025
Microglial
activation
is
the
initial
pathological
event
that
occurs
in
demyelination,
a
prevalent
feature
various
neurological
diseases.
G
protein-coupled
estrogen
receptor
(GPER1),
which
highly
expressed
microglia,
has
been
reported
to
reduce
myelin
damage.
However,
precise
molecular
mechanisms
involved
remain
unclear.
In
this
study,
cuprizone
(CPZ)
-induced
demyelination
model
was
used
investigate
relationship
between
GPER1
and
sheath
injury
its
mechanism.
The
results
demonstrated
deficiency
exacerbated
cognitive
impairment
mice.
Along
with
more
severe
damage
as
well
fewer
oligodendrocytes.
Moreover,
not
only
directly
reduced
number
of
microglia
CPZ
mice,
but
also
caused
iron
ions
overload
debris
induced
vitro.
Transcriptomic,
biological,
morphological
analyses
revealed
microglial
ferroptosis
by
contributes
reduction
number.
summary,
these
findings
can
regulate
through
microglia.
Heliyon,
Journal Year:
2025,
Volume and Issue:
11(4), P. e42688 - e42688
Published: Feb. 1, 2025
Obstructive
pulmonary
diseases,
including
asthma
and
chronic
obstructive
disease,
present
significant
global
public
health
challenges
substantially
impair
patients'
quality
of
life.
Research
indicates
that
sex
hormones
brain-derived
neurotrophic
factor
(BDNF)
are
pivotal
in
regulating
airway
function
inflammatory
responses.
Specifically,
modulate
the
expression
BDNF
through
their
receptors,
namely
estrogen
receptors
androgen
receptors.
Conversely,
enhances
cell
survival
exerts
anti-inflammatory
antioxidant
effects,
influencing
functionality
hormone
This
review
elucidates
interactions
between
emphasizing
synergistic
roles
managing
inflammation,
facilitating
tissue
repair,
mitigating
oxidative
stress.
Through
a
thorough
examination
these
mechanisms,
this
aims
to
foster
more
profound
comprehension
potential
therapeutic
implications
for
management
diseases.
ACS Applied Materials & Interfaces,
Journal Year:
2025,
Volume and Issue:
17(19), P. 27923 - 27936
Published: May 2, 2025
Platelet-rich
plasma-derived
exosomes
(PRP-Exos)
have
recently
been
considered
an
optimized
strategy
for
diabetic
wound
treatment,
yet
the
potential
role
of
PRP-Exos
in
healing
is
still
unclear.
This
study
aims
to
investigate
mechanisms
and
utilize
hydrogel
Pluronic
F127
as
a
carrier
maintain
sustained
release
encapsulated
PRP-Exos.
were
isolated
from
blood
healthy
individuals
characterized,
followed
by
co-culturing
with
human
skin
fibroblasts
(Diabetes
HSF).
RNA
sequencing
(RNA-seq)
was
used
analyze
effect
on
transcriptome
normal
Diabetes
HSF,
screening
validating
crucial
mechanism
target
gene.
Then,
composed
(PRP-Exos/Gel)
constructed
applied
mouse
models
evaluate
mechanism.
RNA-seq
analysis
revealed
that
significantly
upregulated
expression
FosB
HSF.
Further
intervention
HSF
showed
knocking
down
induced
ferroptosis
characterized
decreased
cell
viability,
increased
oxidative
stress,
iron
ion
levels,
along
downregulation
GPX4
SLC7A11
expression,
while
ACSL4
increased;
conversely,
overexpression
had
opposite
effect.
Subsequently,
adding
FosB-knocked
weakened
inhibitory
fibroblasts.
The
synthesized
PRP-Exos/Gel
exhibited
significant
thermosensitivity
exosomes.
In
animal
experiments,
anti-inflammatory
effects,
evidenced
proportion
M2
macrophages
central
granule
cells
tissue,
inhibited
fibroblast
ferroptosis,
thereby
accelerating
healing.
Overall,
displays
continuous
promotes
suppressing
inflammatory
responses
which
provides
new
insights
methods
treatment
wounds.
