International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(15), P. 8212 - 8212
Published: July 27, 2024
Ferroptosis
is
a
form
of
iron-dependent
regulated
cell
death
caused
by
the
accumulation
lipid
peroxides.
In
this
review,
we
summarize
research
on
impact
ferroptosis
disease
models
and
isolated
cells
in
various
types
arthritis.
While
most
studies
have
focused
rheumatoid
arthritis
(RA)
osteoarthritis
(OA),
there
limited
spondylarthritis
crystal
arthropathies.
The
effects
inducing
or
inhibiting
strongly
depend
studied
type.
search
for
new
therapeutic
targets,
chondrocytes
might
promising
any
type
On
other
hand,
induction
may
also
lead
to
desired
decrease
synovial
fibroblasts
RA.
Thus,
must
consider
cell-type-specific
Further
investigation
needed
clarify
these
complexities.
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
Journal of Orthopaedic Translation,
Journal Year:
2024,
Volume and Issue:
44, P. 114 - 124
Published: Jan. 1, 2024
Osteoarthritis
(OA)
is
the
most
common
age-related
musculoskeletal
disease.
However,
there
still
a
lack
of
therapy
that
can
modify
OA
progression
due
to
complex
pathogenic
mechanisms.
The
aim
study
was
explore
role
and
mechanism
XJB-5-131
inhibiting
chondrocytes
ferroptosis
alleviate
progression.
We
treated
tert-butyl
hydroperoxide
(TBHP)-induced
mouse
primary
with
in
vitro.
intracellular
ferroptotic
hallmarks,
cartilage
anabolic
catabolic
markers,
regulatory
genes
proteins
were
detected.
Then
we
established
model
via
destabilization
medial
meniscus
(DMM)
surgery.
mice
intra-articular
injection
regularly
(2
μM,
3
times
per
week).
After
4
8
weeks,
performed
micro-CT
histological
examination
evaluate
protection
subjects.
RNA
sequencing
analysis
unveil
key
downstream
gene
exerting
anti-ferroptotic
effect
OA.
significantly
suppressed
TBHP-induced
increases
hallmarks
(ROS,
lipid
peroxidation,
Fe2+
accumulation),
drivers
(Ptgs2,
Pgd,
Tfrc,
Atf3,
Cdo1),
while
restored
expression
suppressors
(Gpx4,
Fth1).
evidently
promoted
decreased
markers.
Moreover,
inhibited
Cox2
Mmp13,
Col2a1,
Gpx4
Fth1
DMM-induced
articular
cartilage.
Further,
identified
Pebp1
as
potential
target
by
analysis.
anti-ferroptosis
chondroprotective
effects
diminished
Locostatin,
specific
antagonist
Pebp1.
protects
from
DMM
surgery-induced
restoring
therapeutic
drug
management
Journal of Nanobiotechnology,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: May 13, 2024
Abstract
Excessive
production
of
reactive
oxygen
species
(ROS)
and
inflammation
are
the
key
problems
that
impede
diabetic
wound
healing.
In
particular,
dressings
with
ROS
scavenging
capacity
play
a
crucial
role
in
process
chronic
Herein,
Zr-based
large-pore
mesoporous
metal–organic
frameworks
(mesoMOFs)
were
successfully
developed
for
construction
spatially
organized
cascade
bioreactors.
Natural
superoxide
dismutase
(SOD)
an
artificial
enzyme
these
hierarchical
mesoMOFs,
forming
antioxidant
defense
system,
presenting
efficient
intracellular
extracellular
performance.
vivo
experiments
demonstrated
SOD@HMUiO-MnTCPP
nanoparticles
(S@M@H
NPs)
significantly
accelerated
Transcriptomic
western
blot
results
further
indicated
nanocomposite
could
inhibit
fibroblast
senescence
ferroptosis
as
well
stimulator
interferon
genes
(STING)
signaling
pathway
activation
macrophages
mediated
by
mitochondrial
oxidative
stress
through
elimination.
Thus,
biomimetic
multi-enzyme
catalytic
system
spatial
ordering
high
potential
healing,
where
senescence,
ferroptosis,
STING
pathways
may
be
targets.
Graphical
Journal of Nanobiotechnology,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: Jan. 22, 2025
Osteoarthritis
(OA)
is
a
degenerative
joint
disease
with
an
immense
unmet
medical
need.
FGF18
protein
potential
regenerative
factor
for
cartilage
repair.
However,
traditional
delivery
methods
have
limited
efficacy
due
to
the
short
lifetime
and
shallow
infiltration.
In
this
work,
we
discovered
that
lipid
nanoparticle
(LNP)
can
infiltrate
deliver
mRNA
deeper
in
than
proteins.
After
UTR
optimization
chemical
modification,
expression
of
last
up
6
days
cartilage.
Furthermore,
delivering
activates
FOXO3a-autophagy
pathway,
which
protects
against
chondrocyte
degeneration
senescence.
Local
intra-articular
injection
mRNA-LNP
significantly
alleviates
OA
symptoms
DMM
senile
models.
Sustained
accessibility
FGF18-mRNA
chondrocytes
makes
LNP-mRNA
more
effective
recombinant
protein.
summary,
study
presents
novel
approach
superior
alone
holds
promise
as
new
therapeutic
strategy
OA.
Frontiers in Immunology,
Journal Year:
2023,
Volume and Issue:
14
Published: Nov. 8, 2023
Life
expectancy
is
increasing
throughout
the
world
and
coincides
with
a
rise
in
non-communicable
diseases
(NCDs),
especially
for
metabolic
disease
that
includes
diabetes
mellitus
(DM)
neurodegenerative
disorders.
The
debilitating
effects
of
disorders
influence
entire
body
significantly
affect
nervous
system
impacting
greater
than
one
billion
people
disability
peripheral
as
well
cognitive
loss,
now
seventh
leading
cause
death
worldwide.
Metabolic
disorders,
such
DM,
neurologic
remain
significant
challenge
treatment
care
individuals
since
present
therapies
may
limit
symptoms
but
do
not
halt
overall
progression.
These
clinical
challenges
to
address
interplay
between
warrant
innovative
strategies
can
focus
upon
underlying
mechanisms
aging-related
oxidative
stress,
cell
senescence,
death.
Programmed
pathways
involve
autophagy,
apoptosis,
ferroptosis,
pyroptosis
play
critical
role
oversee
processes
include
insulin
resistance,
β-cell
function,
mitochondrial
integrity,
reactive
oxygen
species
release,
inflammatory
activation.
silent
mating
type
information
regulation
2
homolog
1
Advanced Science,
Journal Year:
2024,
Volume and Issue:
11(40)
Published: Sept. 3, 2024
Abstract
A
short
peptide
termed
NEMO‐binding
domain
(NBD)
has
an
inhibitory
effect
on
nuclear
factor
kappa‐B
(NF‐κB).
Despite
its
efficacy
in
inhibiting
inflammatory
responses,
the
precise
neuroprotective
mechanisms
of
NBD
spinal
cord
injury
(SCI)
remain
unclear.
This
study
aims
to
determine
whether
pyroptosis‐related
aspects
involved
effects
post‐SCI.Using
RNA
sequencing,
molecular
SCI
are
explored.
The
evaluation
functional
recovery
is
performed
using
Basso
mouse
scale,
Nissl
staining,
footprint
analysis,
Masson's
trichrome
and
HE
staining.
Western
blotting,
enzyme‐linked
immunosorbent
assays,
immunofluorescence
assays
used
examine
pyroptosis,
autophagy,
lysosomal
membrane
permeabilization
(LMP),
acid
sphingomyelinase
(ASMase),
NF‐κB/p38‐MAPK
related
signaling
pathway.NBD
mitigated
glial
scar
formation,
reduced
motor
neuron
death,
enhanced
mice.
Additionally,
inhibits
ameliorate
LMP‐induced
autophagy
flux
disorder
post‐SCI.
Mechanistically,
alleviates
LMP
subsequently
enhances
by
ASMase
through
NF‐κB/p38‐MAPK/Elk‐1/Egr‐1
cascade,
thereby
mitigating
neuronal
death.
contributes
restoration
suppressing
ASMase‐mediated
depression,
pyroptosis
following
SCI,
which
may
have
potential
clinical
application
value.
Cells,
Journal Year:
2023,
Volume and Issue:
12(22), P. 2595 - 2595
Published: Nov. 9, 2023
Metabolic
disorders
and
diabetes
(DM)
impact
more
than
five
hundred
million
individuals
throughout
the
world
are
insidious
in
onset,
chronic
nature,
yield
significant
disability
death.
Current
therapies
that
address
nutritional
status,
weight
management,
pharmacological
options
may
delay
but
cannot
alter
disease
course
or
functional
organ
loss,
such
as
dementia
degeneration
of
systemic
bodily
functions.
Underlying
these
challenges
onset
aging
associated
with
increased
lifespan,
telomere
dysfunction,
oxidative
stress
generation
lead
to
multi-system
dysfunction.
These
hurdles
point
urgent
need
underlying
mechanisms
innovative
applications.
New
treatment
strategies
involve
non-coding
RNA
pathways
microRNAs
(miRNAs)
circular
ribonucleic
acids
(circRNAs),
Wnt
signaling,
Wnt1
inducible
signaling
pathway
protein
1
(WISP1)
dependent
upon
programmed
cell
death
pathways,
cellular
metabolic
AMP-activated
kinase
(AMPK)
nicotinamide,
growth
factor
Non-coding
RNAs,
AMPK
cornerstone
for
overseeing
complex
offer
avenues
DM
will
necessitate
continued
appreciation
ability
each
independently
unison
influence
clinical
outcome.
