Expert Opinion on Therapeutic Targets,
Journal Year:
2024,
Volume and Issue:
unknown, P. 1 - 27
Published: Dec. 23, 2024
Introduction
Ischemic
stroke
(IS),
a
major
cause
of
mortality
and
disability
worldwide,
remains
significant
healthcare
challenge
due
to
limited
therapeutic
options.
Ferroptosis,
distinct
iron-dependent
form
regulated
cell
death
characterized
by
lipid
peroxidation
oxidative
stress,
has
emerged
as
crucial
mechanism
in
IS
pathophysiology.
This
review
explores
the
role
ferroptosis
its
potential
for
driving
innovative
strategies.
Molecular Medicine,
Journal Year:
2025,
Volume and Issue:
31(1)
Published: March 12, 2025
Abstract
Chemoresistance
continues
to
pose
a
significant
challenge
in
managing
colorectal
cancer
(CRC),
resulting
unfavorable
outcomes
for
patients.
Recent
findings
indicate
that
ferroptosis,
an
innovative
type
of
regulated
cell
death,
might
influence
chemoresistance.
In
this
research,
we
explored
how
WW
domain-binding
protein
1
(WBP1)
affects
mitochondrial
function,
growth,
and
chemoresistance
CRC
cells.
By
employing
both
genetic
pharmacological
methods,
found
WBP1
is
essential
maintaining
respiration
depletion
impaired
leading
reduced
proliferation
increased
ferroptosis.
Exogenous
mitochondria
from
wild-type
cells
restored
proliferation,
suppressed
ferroptosis
WBP1-deficient
cells,
indicating
function
acts
downstream
WBP1.
Importantly,
demonstrated
targeting
or
its
mediated
sensitized
chemoresistant
5-fluorouracil
oxaliplatin
by
inducing
Furthermore,
analyzed
transcriptome
data
patients,
which
indicated
expression
correlated
with
poor
patients
receiving
chemotherapy,
thus
highlighting
the
clinical
significance
our
observations.
Collectively,
results
pinpoint
as
modulator
imply
may
represent
viable
approach
tackling
These
insights
offer
deeper
understanding
molecular
pathways
underlying
guide
development
new
treatment
options.
Journal of Inflammation Research,
Journal Year:
2024,
Volume and Issue:
Volume 17, P. 11631 - 11657
Published: Dec. 1, 2024
Rheumatoid
arthritis
(RA)
is
an
inflammatory
autoimmune
disease,
primarily
characterized
by
chronic
symmetric
synovial
inflammation
and
erosive
bone
destruction.Mitochondria,
the
primary
site
of
cellular
energy
production,
play
a
crucial
role
in
metabolism
possess
homeostatic
regulation
capabilities.
Mitochondrial
function
influences
differentiation,
activation,
survival
both
immune
non-immune
cells
involved
RA
pathogenesis.
If
organism
experiences
hypoxia,
genetic
predisposition,
oxidative
stress,
it
leads
to
mitochondrial
dysfunction,
which
further
affects
cell
metabolism,
proliferation,
apoptosis,
signaling,
causing
onset
progression
RA;
and,
becoming
increasingly
important
treatment
RA.In
this
review,
we
examine
structure
mitochondria,
analyze
potential
causes
dysfunction
RA,
focus
on
mechanisms
triggers
disorders
RA.
We
also
explore
effects
osteoblasts,
emphasizing
its
key
response
processes
Furthermore,
discuss
biological
that
regulate
homeostasis,
are
great
importance
for
prevention
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(24), P. 13279 - 13279
Published: Dec. 11, 2024
Renal
fibrosis
is
a
common
final
pathway
underlying
nearly
almost
all
progressive
kidney
diseases.
Metal
ions
are
essential
trace
elements
in
organisms
and
involved
important
physiological
activities.
However,
aberrations
intracellular
metal
ion
metabolism
may
disrupt
homeostasis,
causing
cell
death
increasing
susceptibility
to
various
Accumulating
evidence
suggests
complex
association
between
metal-dependent
renal
fibrosis.
In
this
article,
we
provide
comprehensive
overview
of
the
specific
molecular
mechanisms
their
crosstalk,
up-to-date
supporting
role
fibrosis,
therapeutic
targeting
strategies,
research
needs,
aiming
offer
rationale
for
future
clinical
treatment
