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.
Cancers,
Journal Year:
2024,
Volume and Issue:
16(6), P. 1220 - 1220
Published: March 20, 2024
Based
on
the
multifaceted
molecular
machinery
that
tightly
controls
iron
cellular
homeostasis,
this
review
delves
into
its
paradoxical,
potentially
dangerous
role
in
biological
systems,
with
a
special
focus
double-edged
sword
correlations
cancer.
Indeed,
though
is
vital
micronutrient
and
required
cofactor
participating
several
essential
cell
functions,
tendency
to
cause
oxidative
stress
can
be
related
both
cancer
risk
activation
of
death
pathways.
In
scenario,
ferroptosis
refers
an
iron-dependent
form
regulated
(RCD)
powered
by
overload
lethal
peroxides
sharing
distinctive
oxidized
phospholipid
profiles.
As
unique
pathway,
morphologically
mechanistically
different
from
other
types
programmed
involving
executioner
family
proteins.
The
accumulation
cytotoxic
lipid
encompasses
antagonism
between
execution
defense
occurring
when
ferroptosis-promoting
activities
significantly
exceed
antioxidant
defenses.
most
recent
breakthroughs
have
aroused
great
consideration
tumor
biology,
as
targeting
provide
new
tools
for
exploring
therapeutic
strategies
suppression.
Mutations
death/survival
pathway
alterations,
well
metabolic
regulations
cells,
including
propensity
generate
ROS,
are
seen
features
render
cells
unprotected
ferroptosis,
thereby
exposing
vulnerabilities
which
deserve
further
attention
regarded
targetable
cancers
limited
options.
International Journal of Nanomedicine,
Journal Year:
2025,
Volume and Issue:
Volume 20, P. 1637 - 1659
Published: Feb. 1, 2025
Abstract:
Kidney
diseases
are
a
significant
global
cause
of
death
and
disability,
resulting
from
the
destruction
kidney
structure
function
due
to
an
imbalance
between
renal
parenchymal
cells
proliferation
or
recruitment
maladaptive
cells,
caused
by
various
pathogenic
factors.
Currently,
therapies
their
efficacy
for
limited.
Ferroptosis
is
newly
discovered
iron-dependent
regulated
cell
death.
The
iron
homeostasis
lipid
metabolism
affects
occurrence
progression
triggering
ferroptosis,
which
considered
important
target
development
disease
drugs.
However,
in
clinical
practice,
targeted
ferroptosis
therapy
faces
obstacles
such
as
poor
drug
solubility,
low
resistance,
imprecise
targeting.
With
rapid
nanomaterials
medical
field,
new
opportunities
have
emerged
precise
regulation
treatment
diseases.
This
article
provides
detailed
introduction
regulatory
mechanisms
properties
nanomaterials,
application
diseases,
with
focus
on
discussing
action
therapeutic
potential
based
aim
this
provide
ideas
directions
future
treatments.
Keywords:
nanomaterial,
nanomedicine,
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: April 11, 2025
Abstract
Both
cancer
patients
receiving
radiotherapy
and
civilians
in
a
mass
casualty
nuclear
event
may
suffer
from
radiation
induced
damage
to
organ
systems.
Radiation
liver
disease
(RILD)
can
cause
acute
long-term
dysfunction
that
potentially
leads
death.
The
objective
of
this
study
was
ascertain
the
validity
quad-culture
chip,
micro-physiological
system
comprising
primary
human
hepatocytes
non-parenchymal
cells
(NPCs),
including
sinusoidal
endothelial
cells,
hepatic
stellate
(HSCs),
Kupffer
as
model
for
RILD.
exposure
chip
resulted
DNA
cellular
senescence
NPCs.
We
observed
metabolic
dysfunction,
inflammation,
HSCs
activation.
Whole
genome
sequencing
revealed
gene
alterations
pathways
relevant
RILD,
well
potential
efficacy
N
-acetylcysteine
amide
(NACA)
against
NACA
exhibited
capacity
mitigate
decreased
impact
on
other
pathophysiological
changes.
CDKN1A
miR-34a-5p
were
validated
useful
response
treatment
biomarkers.
These
findings
highlight
an
effective
investigating
microenvironment
RILD
evaluating
therapeutic
countermeasures
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(8), P. 3852 - 3852
Published: April 18, 2025
Cancer
drug
resistance
occurs
when
cancer
cells
evade
cell
death
following
treatment
with
chemotherapy,
radiation
therapy,
and
targeted
therapies.
This
is
often
linked
to
the
reprogramming
of
programmed
(PCD)
pathways,
allowing
survive
drug-induced
stress.
However,
certain
anticancer
therapies,
combined
specific
agents
or
inhibitors,
can
induce
ferroptosis—a
form
driven
by
iron-dependent
lipid
peroxidation.
Currently,
extensive
preclinical
clinical
research
underway
investigate
molecular,
cellular,
tissue-specific
mechanisms
underlying
ferroptosis,
goal
identifying
strategies
overcome
in
cancers
unresponsive
conventional
PCD
pathways.
By
harnessing
be
compelled
undergo
peroxidation-induced
death,
potentially
improving
therapeutic
outcomes
patients
cancer.
short
review
aims
enhance
understanding
ferroptosis
inducers
therapy
stimulate
further
into
ferroptosis-based
approaches
for
more
effective
treatment.
Clinical and Translational Medicine,
Journal Year:
2025,
Volume and Issue:
15(5)
Published: May 1, 2025
Abstract
Background
Hepatocellular
carcinoma
remains
one
of
the
most
lethal
cancers,
characterized
by
poor
prognosis
and
low
life
expectancy.
Unfortunately,
there
are
very
few
molecular
therapeutic
options
available
for
it.
Sorafenib
is
a
current
standard
first‐line
treatment
advanced
hepatocellular
carcinoma,
however,
drug
resistance
significantly
limits
its
efficacy.
Methods
Ubiquitin‐specific
protease
22
(USP22)
expression
level
prognostic
significance
in
were
analyzed
using
The
Cancer
Genome
Atlas
(TCGA)
database.
A
series
cellular
experiments
related
to
cell
proliferation
ferroptosis,
mouse
tumor‐bearing
performed
investigate
role
USP22
growth
resistance.
Flag
affinity
purification
coupled
with
mass
spectrometry,
co‐immunoprecipitation,
ubiquitination
assays
conducted
identify
direct
substrates
USP22.
Spike‐in
chromatin‐immunoprecipitation
(ChIP)‐seq,
RNA‐seq,
ChIP
employed
explore
transcriptional
as
an
H2BK120ub
deubiquitinase.
Results
Analysis
TCGA
database
reveals
that
highly
expressed
tissues,
which
closely
associated
patient
prognosis.
Our
data
further
indicates
promotes
cells
via
deubiquitinating
stabilizing
cyclin‐dependent
kinase
11B
(CDK11B).
Additionally,
acts
novel
inducer
suppresses
Sorafenib‐triggered
ferroptosis
cells.
It
reduces
transcription
transferrin
receptor
(TFRC)
decreasing
occupancy
at
TFRC
start
site
(TSS)
downstream
region,
thereby
inhibiting
upon
treatment.
Finally,
animal
confirm
promoting
vivo.
Taken
together,
this
study
demonstrates
inhibits
Sorafenib‐induced
non‐histone
substrate
CDK11B
histone
H2B,
respectively.
Conclusions
findings
suggest
promising
biomarker
target
patients,
particularly
those
Key
points
CDK11B.
enhances
through
USP22/H2BK120ub/TFRC
axis.
