Journal of Trace Elements in Medicine and Biology,
Journal Year:
2025,
Volume and Issue:
88, P. 127611 - 127611
Published: Feb. 3, 2025
Iron
homeostasis
has
a
significant
impact
on
the
phenotypic
transformation
of
macrophages
and
is
implicated
in
various
diseases.
In
this
study,
we
evaluated
effect
cystathionine-gamma-lyase
(CSE)/transsulfuration
pathway
iron-overload
induced
macrophage
phenotype
change.
The
biochemical
parameters,
such
as
qRT-PCR,
western
blot,
fluorescence
staining,
were
assessed
both
vitro
vivo.
overload
disrupts
iron
metabolism
alters
expression
genes
involved
transport,
resulting
polarization
towards
M1
an
alternating
activation
state
M2.
Meanwhile,
excessive
led
to
increase
lipid
peroxidation
levels
disrupted
cysteine
metabolism.
By
utilizing
erastin
inhibit
SLC7A11
activity
block
exogenous
uptake,
able
observe
exacerbation
proinflammatory
under
conditions
deprivation.
CSE/transsulfuration
pathway,
serves
primary
route
for
endogenous
synthesis.
presence
overload,
CSE
was
upregulated
further
enhanced
by
Deletion
CSE-knockout
mice
exacerbated
inflammatory
transition
iron-overloaded
impacting
ferritinophagy.
regulated
change
iron-overload,
which
may
offer
novel
insights
into
potential
therapeutic
strategies
overload-related
disorders.
Oxidative Medicine and Cellular Longevity,
Journal Year:
2023,
Volume and Issue:
2023, P. 1 - 14
Published: Jan. 17, 2023
It
was
found
recently
that
iron
overload
can
cause
osteoporosis
in
rats.
Through
vitro
and
vivo
experimentations,
the
purpose
of
present
study
to
validate
confirm
inhibitory
effects
melatonin
on
death
its
role
bone
microstructure
improvements.
Melatonin
(100
mol/L)
administered
MC3T3-E1
cells
induced
by
for
48
hours.
The
expression
cleaved
caspase-3
PARP
production
ROS
(reactive
oxygen
species)
mitochondrial
damage
were
all
exacerbated
overload.
On
other
hand,
restored
these
impacts
produced
By
evaluating
PI3K/AKT/GSK-3β/P70S6k
signaling
pathway-related
proteins
(RUNX2,
BMP2,
ALP,
OCN)
using
RT-PCR
Western
blot,
osteogenic-related
identified.
Alizarin
red
S
alkaline
phosphatase
utilized
evaluate
osteogenic
potential
cells.
significantly
improved
ability
phosphorylation
rates
PI3K,
AKT,
GSK-3β,
P70S6k
overload-induced
In
vivo,
treated
osteoporotic
defect
Rat
skeletal
observed
micro-CT
tissue
pathological
section
staining.
ELISA
identify
OCN,
PINP,
CTX-I,
SI
serum
We
discovered
increased
trabecular
regeneration
repair
defects
caused
conclusion,
enhanced
activating
pathway
promoting
healing
Frontiers in Cell and Developmental Biology,
Journal Year:
2023,
Volume and Issue:
11
Published: Feb. 3, 2023
Ferroptosis
is
a
novel
type
of
cell
death
associated
with
iron
accumulation
and
excessive
lipid
peroxidation.
Elucidating
the
underlying
molecular
mechanisms
ferroptosis
intensively
related
to
development
treatment
multiple
diseases,
including
musculoskeletal
disorders.
Moreover,
in
vitro
vivo
studies
have
shown
importance
oxidative
stress
conditions
such
as
osteoporosis,
osteoarthritis,
rheumatoid
arthritis,
osteosarcoma.
Ferroptosis-derived
clinical
management
diseases
offers
tremendous
attractive
opportunities.
Notably,
agonists
been
proven
enhance
sensitivity
osteosarcoma
cells
conventional
therapeutic
strategies.
In
this
review,
we
mainly
focused
on
implications
regulation
pathophysiology
response
Understanding
roles
for
controlling
might
provide
directions
ferroptosis-driven
therapies,
which
could
be
promising
Biomolecules,
Journal Year:
2024,
Volume and Issue:
14(11), P. 1369 - 1369
Published: Oct. 28, 2024
Endoplasmic
reticulum
(ER)
stress
is
a
cellular
phenomenon
that
arises
in
response
to
the
accumulation
of
misfolded
proteins
within
ER.
This
process
triggers
activation
signalling
pathway
known
as
unfolded
protein
(UPR),
which
aims
restore
ER
homeostasis
by
reducing
synthesis,
increasing
degradation,
and
promoting
proper
folding.
However,
excessive
can
perturb
regular
function
contribute
development
diverse
pathological
conditions.
As
well
known,
ferroptosis
kind
programmed
cell
death
characterized
lipid
peroxides
iron-dependent
reactive
oxygen
species
(ROS),
resulting
oxidative
harm
structures.
In
recent
years,
there
has
been
evidence
indicating
occurs
musculoskeletal
disorders
(MSDs),
with
emerging
recognition
complex
relationship
between
ferroptosis.
review
presents
summary
pathway.
Most
importantly,
it
delves
into
significance
skeletal
or
muscle
types.
Furthermore,
we
highlight
potential
benefits
targeting
correlation
treating
degenerative
MSDs.
Journal of Trace Elements in Medicine and Biology,
Journal Year:
2025,
Volume and Issue:
88, P. 127611 - 127611
Published: Feb. 3, 2025
Iron
homeostasis
has
a
significant
impact
on
the
phenotypic
transformation
of
macrophages
and
is
implicated
in
various
diseases.
In
this
study,
we
evaluated
effect
cystathionine-gamma-lyase
(CSE)/transsulfuration
pathway
iron-overload
induced
macrophage
phenotype
change.
The
biochemical
parameters,
such
as
qRT-PCR,
western
blot,
fluorescence
staining,
were
assessed
both
vitro
vivo.
overload
disrupts
iron
metabolism
alters
expression
genes
involved
transport,
resulting
polarization
towards
M1
an
alternating
activation
state
M2.
Meanwhile,
excessive
led
to
increase
lipid
peroxidation
levels
disrupted
cysteine
metabolism.
By
utilizing
erastin
inhibit
SLC7A11
activity
block
exogenous
uptake,
able
observe
exacerbation
proinflammatory
under
conditions
deprivation.
CSE/transsulfuration
pathway,
serves
primary
route
for
endogenous
synthesis.
presence
overload,
CSE
was
upregulated
further
enhanced
by
Deletion
CSE-knockout
mice
exacerbated
inflammatory
transition
iron-overloaded
impacting
ferritinophagy.
regulated
change
iron-overload,
which
may
offer
novel
insights
into
potential
therapeutic
strategies
overload-related
disorders.
