Journal of Advanced Research,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 1, 2024
Diabetic
osteoporosis
(DOP)
is
an
insidious
complication
of
diabetes
with
limited
therapeutic
options.
DOP
pathologically
associated
various
types
regulated
cell
death,
but
the
precise
role
ferroptosis
in
process
remains
poorly
understood.
Asperosaponin
VI
(AVI),
known
for
its
clinical
efficacy
treating
bone
fractures
and
osteoporosis,
may
exert
osteoprotective
effects
through
mechanisms
involving
ferroptosis,
however
this
has
not
been
established.
Signal Transduction and Targeted Therapy,
Journal Year:
2024,
Volume and Issue:
9(1)
Published: Oct. 14, 2024
Iron,
an
essential
mineral
in
the
body,
is
involved
numerous
physiological
processes,
making
maintenance
of
iron
homeostasis
crucial
for
overall
health.
Both
overload
and
deficiency
can
cause
various
disorders
human
diseases.
Ferroptosis,
a
form
cell
death
dependent
on
iron,
characterized
by
extensive
peroxidation
lipids.
Unlike
other
kinds
classical
unprogrammed
death,
ferroptosis
primarily
linked
to
disruptions
metabolism,
lipid
peroxidation,
antioxidant
system
imbalance.
Ferroptosis
regulated
through
transcription,
translation,
post-translational
modifications,
which
affect
cellular
sensitivity
ferroptosis.
Over
past
decade
or
so,
diseases
have
been
as
part
their
etiology,
including
cancers,
metabolic
disorders,
autoimmune
diseases,
central
nervous
cardiovascular
musculoskeletal
Ferroptosis-related
proteins
become
attractive
targets
many
major
that
are
currently
incurable,
some
regulators
shown
therapeutic
effects
clinical
trials
although
further
validation
potential
needed.
Therefore,
in-depth
analysis
its
molecular
mechanisms
may
offer
additional
strategies
prevention
treatment.
In
this
review,
we
discuss
significance
contribution
etiology
development
along
with
evidence
supporting
targeting
approach.
Importantly,
evaluate
recent
promising
interventions,
providing
guidance
future
targeted
treatment
therapies
against
Advanced Science,
Journal Year:
2024,
Volume and Issue:
11(12)
Published: Jan. 17, 2024
Abstract
Ferroptosis
is
a
necrotic
form
of
iron‐dependent
regulatory
cell
death.
Estrogen
withdrawal
can
interfere
with
iron
metabolism,
which
responsible
for
the
pathogenesis
postmenopausal
osteoporosis
(PMOP).
Here,
it
demonstrated
that
estrogen
induces
accumulation
in
skeleton
and
ferroptosis
osteocytes,
leading
to
reduced
bone
mineral
density.
Furthermore,
facilitatory
effect
osteocytes
verified
occurrence
development
associated
over
activated
osteoclastogenesis
using
direct
osteocyte/osteoclast
coculture
system
glutathione
peroxidase
4
(GPX4)
knockout
ovariectomized
mice.
In
addition,
nuclear
factor
erythroid
derived
2‐related
factor‐2
(Nrf2)
signaling
pathway
confirmed
be
crucial
osteocytic
cells.
Nrf2
regulates
expression
kappa‐B
ligand
(RANKL)
by
regulating
DNA
methylation
level
RANKL
promoter
mediated
methyltransferase
3a
(Dnmt3a),
as
an
important
mechanism
ferroptosis‐mediated
osteoclastogenesis.
Taken
together,
this
data
suggests
involved
PMOP
targeted
tune
homeostasis.
Bone Research,
Journal Year:
2025,
Volume and Issue:
13(1)
Published: Jan. 16, 2025
Abstract
Osteocytes
are
the
main
cells
in
mineralized
bone
tissue.
Elevated
osteocyte
apoptosis
has
been
observed
lytic
lesions
of
patients
with
multiple
myeloma.
However,
their
precise
contribution
to
metastasis
remains
unclear.
Here,
we
investigated
pathogenic
mechanisms
driving
melanoma-induced
death.
Both
vivo
models
and
vitro
assays
were
combined
untargeted
RNA
sequencing
approaches
explore
pathways
governing
We
could
show
that
ferroptosis
is
primary
mechanism
behind
death
context
melanoma
metastasis.
HMOX1
was
identified
as
a
crucial
regulatory
factor
this
process,
directly
involved
inducing
affecting
viability.
uncover
non-canonical
pathway
involves
excessive
autophagy-mediated
ferritin
degradation,
highlighting
complex
relationship
between
autophagy
In
addition,
HIF1α
shown
an
upstream
regulator,
providing
potential
target
for
modulating
expression
influencing
autophagy-dependent
ferroptosis.
conclusion,
our
study
provides
insight
into
induced
by
metastasis,
specific
focus
on
its
regulation.
This
would
enhance
comprehension
Nature Communications,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: Jan. 17, 2025
Oxidative
stress
plays
a
critical
role
in
postmenopausal
osteoporosis,
yet
its
impact
on
osteoblasts
remains
underexplored,
limiting
therapeutic
advances.
Our
study
identifies
phospholipid
peroxidation
as
key
feature
of
osteoporosis.
Estrogen
regulates
the
transcription
glutathione
peroxidase
4
(GPX4),
an
enzyme
crucial
for
reducing
peroxides
osteoblasts.
The
deficiency
estrogen
reduces
GPX4
expression
and
increases
Inhibition
or
knockout
impairs
osteoblastogenesis,
while
elimination
rescues
bone
formation
mitigates
Mechanistically,
4-hydroxynonenal,
end-product
peroxidation,
binds
to
integrin-linked
kinase
triggers
protein
degradation,
disrupting
RUNX2
signaling
inhibiting
osteoblastogenesis.
Importantly,
we
identified
two
natural
allosteric
activators
GPX4,
6-
8-Gingerols,
which
promote
osteoblastogenesis
demonstrate
anti-osteoporotic
effects.
findings
highlight
detrimental
underscore
promising
target
osteoporosis
treatment.
Cell Proliferation,
Journal Year:
2024,
Volume and Issue:
57(10)
Published: May 19, 2024
Abstract
Cortical
bone
loss
is
intricately
associated
with
ageing
and
coincides
iron
accumulation.
The
precise
role
of
ferroptosis,
characterized
by
overload
lipid
peroxidation,
in
senescent
osteocytes
remains
elusive.
We
found
that
ferroptosis
was
a
crucial
mode
osteocyte
death
cortical
during
ageing.
Using
single‐cell
transcriptome
analysis,
we
identified
activating
transcription
factor
3
(ATF3)
as
critical
driver
ferroptosis.
Elevated
ATF3
expression
promotes
uptake
upregulating
transferrin
receptor
1
while
simultaneously
inhibiting
solute
carrier
family
7‐member
11‐mediated
cystine
import.
This
process
leads
to
an
culminating
Importantly,
inhibition
aged
mice
effectively
alleviated
the
mitigated
mass
loss.
Taken
together,
our
findings
establish
pivotal
older
adults,
providing
promising
prevention
treatment
strategies
for
osteoporosis
fractures.
Biomedicines,
Journal Year:
2025,
Volume and Issue:
13(1), P. 170 - 170
Published: Jan. 13, 2025
Background/Objectives:
Periprosthetic
osteolysis
is
the
primary
cause
of
arthroplasty
failure
in
majority
patients.
Mechanistically,
wear
debris
released
from
articulating
surfaces
a
prosthesis
initiates
local
inflammation
and
several
modes
regulated
cell
death
programs,
such
as
ferroptosis,
which
represents
promising
therapeutic
target
various
chronic
inflammatory
diseases.
Thus,
current
study
aimed
at
exploring
potential
targeting
ferroptosis
polyethylene-wear-debris-induced
model.
Methods:
Inverted
culture
model
was
used
for
stimulating
cells
with
vitro,
calvarial
evaluating
effects
inhibitors
vivo.
Results:
The
immunostaining
periprosthetic
bone
tissues
demonstrated
number
osteocytes
expressing
markers.
Likewise,
expressions
markers
were
confirmed
polyethylene-wear-debris-stimulated
osteocyte-like
osteoblasts
direct
stimulation
but
not
an
indirect
Furthermore,
polyethylene
implanted
onto
mice
treated
DFO
Fer-1.
These
treatments
alleviated
pathological
resorption
induced
by
implantation.
Conclusions:
Our
data
broaden
knowledge
pathogenesis
highlight
target.
