Abstract
Macrophages
undergo
plasma
membrane
fusion
and
cell
multinucleation
to
form
multinucleated
giant
cells
(MGCs)
such
as
osteoclasts
in
bone,
Langhans
(LGCs)
part
of
granulomas
or
foreign‐body
(FBGCs)
reaction
exogenous
material.
How
per
se
contributes
functional
specialization
mature
mononuclear
macrophages
remains
poorly
understood
humans.
Here,
we
integrate
comparative
transcriptomics
with
assays
purified
human
osteoclasts,
LGCs
FBGCs.
Strikingly,
all
three
types
MGCs,
causes
a
pronounced
downregulation
macrophage
identity.
We
show
enhanced
lysosome‐mediated
intracellular
iron
homeostasis
promoting
MGC
formation.
The
transition
from
multinuclear
state
is
accompanied
by
specific
each
polykaryon.
Enhanced
phagocytic
mitochondrial
function
associate
FBGCs
respectively.
Moreover,
preferentially
express
B7‐H3
(CD276)
can
granuloma‐like
clusters
vitro
,
suggesting
that
their
potentiates
T
activation.
These
findings
demonstrate
how
cell–cell
reset
identity
an
advanced
maturation
step
confers
MGC‐specific
functionality.
Abstract
Ferroptosis,
a
unique
type
of
cell
death,
is
characterized
by
iron-dependent
accumulation
and
lipid
peroxidation.
It
closely
related
to
multiple
biological
processes,
including
iron
metabolism,
polyunsaturated
fatty
acid
the
biosynthesis
compounds
with
antioxidant
activities,
glutathione.
In
past
10
years,
increasing
evidence
has
indicated
potentially
strong
relationship
between
ferroptosis
onset
progression
age-related
orthopedic
diseases,
such
as
osteoporosis
osteoarthritis.
Therefore,
in-depth
knowledge
regulatory
mechanisms
in
diseases
may
help
improve
disease
treatment
prevention.
This
review
provides
an
overview
recent
research
on
its
influences
bone
cartilage
homeostasis.
begins
brief
systemic
metabolism
ferroptosis,
particularly
potential
ferroptosis.
presents
discussion
role
promotion
loss
degradation
inhibition
osteogenesis.
Finally,
it
focuses
future
targeting
treat
intention
inspiring
further
clinical
development
therapeutic
strategies.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(2), С. 1024 - 1024
Опубликована: Янв. 13, 2024
Periodontitis
is
a
chronic
infectious
disorder
damaging
periodontal
tissues,
including
the
gingiva,
ligament,
cementum,
and
alveolar
bone.
It
arises
from
complex
interplay
between
pathogenic
oral
bacteria
host
immune
response.
Contrary
to
previous
view
of
“energy
factories”,
mitochondria
have
recently
been
recognized
as
semi-autonomous
organelles
that
fine-tune
cell
survival,
death,
metabolism,
other
functions.
Under
physiological
conditions,
tissue
cells
participate
in
dynamic
processes,
differentiation,
mineralization,
regeneration.
These
fundamental
activities
depend
on
properly
functioning
mitochondria,
which
play
crucial
role
through
bioenergetics,
dynamics,
mitophagy,
quality
control.
However,
during
initiation
progression
periodontitis,
mitochondrial
control
compromised
due
range
challenges,
such
bacterial–host
interactions,
inflammation,
oxidative
stress.
Currently,
mounting
evidence
suggests
dysfunction
serves
common
pathological
mechanism
linking
periodontitis
with
systemic
conditions
like
type
II
diabetes,
obesity,
cardiovascular
diseases.
Therefore,
targeting
intervene
multiple
associated
diseases
holds
great
therapeutic
potential.
This
review
provides
advanced
insights
into
Moreover,
we
emphasize
significance
diverse
modulators
signaling
pathways
regulate
function
cells.
Abstract
Postmenopausal
osteoporosis
is
one
of
the
most
prevalent
skeletal
disorders
in
women
and
featured
by
imbalance
between
intraosseous
vascularization
bone
metabolism.
In
this
study,
a
pH‐responsive
shell–core
structured
micro/nano‐hydrogel
microspheres
loaded
with
polyhedral
oligomeric
silsesquioxane
(POSS)
using
gas
microfluidics
ionic
cross‐linking
technology
are
developed.
This
microsphere
system
(PDAP@Alg/Cs)
can
achieve
oral
delivery,
intragastric
protection,
intestinal
slow/controlled
release,
active
targeting
to
tissue,
thus
negatively
affecting
angiogenesis
osteoclastogenesis.
According
biodistribution
data,
PDAP@Alg/Cs
successfully
enhance
drug
absorption
bioavailability
through
intestine
adhesion
after
administration.
vitro
vivo
experiments
reveal
that
promoted
type
H
vessel
formation
inhibited
resorption,
effectively
mitigating
loss
activating
HIF‐1
α
/VEGF
signaling
pathway
promoting
heme
oxygenase‐1
(HO‐1)
expression.
conclusion,
novel
simultaneously
accelerate
decrease
offering
brand‐new
approach
prevent
postmenopausal
osteoporosis.
Biomolecules,
Год журнала:
2023,
Номер
13(6), С. 1006 - 1006
Опубликована: Июнь 17, 2023
The
objective
of
the
present
study
was
to
review
recent
epidemiological
and
clinical
data
on
association
between
selected
minerals
trace
elements
osteoporosis,
as
well
discuss
molecular
mechanisms
underlying
these
associations.
We
have
performed
a
search
in
PubMed-Medline
Google
Scholar
databases
using
MeSH
terms
"osteoporosis",
"osteogenesis",
"osteoblast",
"osteoclast",
"osteocyte"
with
names
particular
through
21
March
2023.
demonstrate
that
physiological
nutritional
levels
promote
osteogenic
differentiation
up-regulation
BMP-2
Wnt/β-catenin
signaling,
other
pathways.
miRNA
epigenetic
effects
were
also
involved
regulation
minerals.
antiresorptive
effect
associated
inhibition
osteoclastogenesis.
At
same
time,
bone
health
appeared
be
dose-dependent
low
doses
promoting
an
effect,
whereas
high
exerted
opposite
which
promoted
resorption
impaired
formation.
Concomitant
results
laboratory
studies,
several
trials
studies
demonstrated
supplementation
Zn,
Mg,
F,
Sr
may
improve
quality,
thus
inducing
antiosteoporotic
effects.
Journal of Clinical Medicine,
Год журнала:
2024,
Номер
13(16), С. 4679 - 4679
Опубликована: Авг. 9, 2024
The
complex
relationship
between
trace
elements
and
skeletal
health
has
received
increasing
attention
in
the
scientific
community.
Among
these
minerals,
manganese
(Mn)
emerged
as
a
key
element
affecting
bone
metabolism
integrity.
This
review
examines
multifaceted
role
of
Mn
health,
including
its
effects
on
regeneration,
mineralization,
overall
strength.
article
is
based
synthesis
experimental
models,
epidemiologic
studies,
clinical
trials
mechanisms
effect
metabolism.
Current
research
data
show
that
actively
involved
processes
remodeling
by
modulating
activity
osteoblasts
osteoclasts,
well
main
cells
regulate
formation
resorption.
ions
have
profound
mineralization
density
intricately
regulating
signaling
pathways
enzymatic
reactions
cells.
Additionally,
superoxide
dismutase
(MnSOD),
located
mitochondria,
plays
crucial
osteoclast
differentiation
function,
protecting
osteoclasts
from
oxidative
damage.
Understanding
nuances
Mn’s
interaction
with
essential
for
optimizing
strategies,
potentially
preventing
managing
diseases.
Key
findings
include
stimulation
osteoblast
proliferation
differentiation,
inhibition
osteoclastogenesis,
preservation
mass
through
RANK/RANKL/OPG
pathway.
These
results
underscore
importance
maintaining
highlight
need
further
into
therapeutic
potential.
Frontiers in Immunology,
Год журнала:
2025,
Номер
16
Опубликована: Март 17, 2025
Bone
remodeling
is
a
dynamic
and
continuous
process
involving
three
components:
bone
formation
mediated
by
osteoblasts,
resorption
osteoclasts,
formation-resorption
balancing
regulated
osteocytes.
Excessive
osteocyte
death
found
in
various
diseases,
such
as
postmenopausal
osteoporosis
(PMOP),
osteoclasts
are
increased
activated
at
sites.
Currently,
apart
from
apoptosis
necrosis
previously
established,
more
forms
of
cell
reported,
including
necroptosis,
ferroptosis
pyroptosis.
These
play
important
role
the
development
inflammatory
diseases
diseases.
Increasing
studies
have
revealed
that
promote
osteoclast
via
different
mechanism,
actively
secreting
pro-inflammatory
pro-osteoclastogenic
cytokines,
tumor
factor
alpha
(TNF-α)
receptor
activator
nuclear
factor-kappa
B
ligand
(RANKL),
or
passively
releasing
damage
associated
molecule
patterns
(DAMPs),
high
mobility
group
box
1
(HMGB1).
This
review
summarizes
established
potential
mechanisms
which
regulate
formation,
aiming
to
provide
better
understanding
disease
therapeutic
target.
