Phytotherapy Research,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Nov. 8, 2024
Degenerative
bone
and
joint
diseases
(DBJDs),
characterized
by
osteoporosis,
osteoarthritis,
chronic
inflammation
of
surrounding
soft
tissues,
are
systemic
conditions
primarily
affecting
the
skeletal
system.
Ferroptosis,
a
programmed
cell
death
pathway
distinct
from
apoptosis,
autophagy,
necroptosis.
Accumulating
evidence
suggests
that
ferroptosis
is
intricately
linked
to
pathogenesis
DBJDs,
targeting
its
regulation
could
be
beneficial
in
managing
these
conditions.
Natural
products,
known
for
their
anti-inflammatory
antioxidant
properties,
have
shown
unique
advantages
preventing
potentially
through
modulating
ferroptosis.
This
article
provides
an
overview
latest
research
on
ferroptosis,
with
focus
role
DBJDs
therapeutic
potential
natural
products
this
pathway,
offering
novel
insights
prevention
treatment
DBJDs.
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
Frontiers in Pharmacology,
Journal Year:
2025,
Volume and Issue:
16
Published: Feb. 13, 2025
Osteoarthritis
is
a
degenerative
joint
disorder
characterized
by
cartilage
degradation,
synovial
inflammation,
and
altered
subchondral
bone
structure.
Recent
insights
have
identified
mitochondrial
dysfunction
as
pivotal
factor
in
OA
pathogenesis,
contributing
to
chondrocyte
apoptosis,
oxidative
stress,
extracellular
matrix
degradation.
Disruptions
dynamics,
including
impaired
biogenesis,
mitophagy,
metabolic
shifts
from
phosphorylation
glycolysis,
exacerbate
damage
promoting
the
production
of
reactive
oxygen
species
matrix-degrading
enzymes
such
ADAMTS
MMPs.
This
review
explores
molecular
mechanisms
underlying
OA,
emphasizing
its
role
homeostasis
inflammation.
Furthermore,
it
highlights
emerging
therapeutic
strategies
targeting
pathways,
antioxidants,
mitophagy
enhancers,
modulators,
potential
interventions
mitigate
disease
progression,
which
offer
promising
avenues
for
advancing
personalized
disease-modifying
treatments
OA.
Journal of Natural Products,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 11, 2025
A
chemical
investigation
of
the
soil-derived
fungus
Trichocladium
sp.
XZ8
led
to
isolation
five
new
indole
alkaloids,
trichindoles
A–E
(1–5),
with
diverse
architectures,
along
seven
known
analogues
(6–12).
Their
structures
were
elucidated
by
extensive
spectroscopic
data
analysis,
and
their
absolute
configurations
determined
single-crystal
X-ray
diffraction
modified
Mosher's
method.
Compound
1
is
a
polyketide-alkaloid
hybrid
incorporating
rare
succinimide
motif,
compound
2
represents
first
example
dimeric
isopentenyl
indole-containing
alkaloid
bridged
propane-1,2-diol
moiety.
Compounds
1,
4,
8,
11,
12
showed
significant
neuroprotective
effects
against
RSL3-induced
ferroptosis
in
PC12
cells
at
10
μM.
Moreover,
4
might
ameliorate
through
regulation
SLC7A11
pathway
ferritinophagy,
suggesting
potential
as
promising
lead
compounds
for
treatment
neurodegenerative
diseases.
Journal of Contemporary Medical Practice,
Journal Year:
2025,
Volume and Issue:
7(1), P. 157 - 162
Published: Jan. 31, 2025
Osteoarthritis
is
a
common
chronic
joint
disease
that
brings
great
pain
and
life
burden
to
patients.
In
recent
years,
ferroptosis,
novel
mode
of
programmed
cell
death,
has
gradually
gained
attention
in
the
pathogenesis
osteoarthritis.
As
traditional
treatment
method,
Chinese
medicine
advantages
multi-targeting
overall
regulation
regulating
ferroptosis
This
review
discusses
mechanisms
TCM
ferroptosis-related
signaling
pathways,
anti-oxidative
stress,
inhibition
inflammatory
responses,
key
regulators
regulatory
pathways
osteoarthritis,
comprehends
current
status
research
on
targeting
active
ingredients
inhibit
so
as
provide
reference
for
mechanism
treating
osteoarthritis
development
drugs.
Journal of Cellular and Molecular Medicine,
Journal Year:
2025,
Volume and Issue:
29(5)
Published: Feb. 27, 2025
ABSTRACT
Ferroptosis
plays
a
crucial
role
in
the
pathogenesis
of
osteoarthritis
(OA),
and
inhibition
chondrocyte
ferroptosis
effectively
alleviates
OA
progression.
Krüppel‐like
factor
9
(KLF9)
is
demonstrated
to
be
upregulated
OA,
but
its
molecular
mechanism
remains
unclear.
The
study
aimed
investigate
KLF9
Primary
chondrocytes
were
treated
with
IL‐1β
establish
an
cell
model,
showed
that
was
highly
expressed
IL‐1β‐incubated
chondrocytes.
Knockdown
alleviated
IL‐1β‐induced
degeneration.
In
addition,
decreased
methylation
proportion
gene
promoter.
DNA
methyltransferase
1
(DNMT1)
directly
bound
promoter,
overexpression
DNMT1
inhibited
expression
by
promoting
promoter
Subsequently,
shRNA
pcDNA‐CYP1B1
individually
or
altogether
transfected
into
Cytochrome
P450
1B1
(CYP1B1)
chondrocytes,
abrogated
inhibitory
effect
on
ferroptosis.
Moreover,
Ferrostatin‐1
(Fer‐1,
inhibitor
ferroptosis)
reversed
promotion
Finally,
vivo
experiments
significantly
suppressed
cartilage
tissue
damage,
ferroptosis,
IHC
scores
CYP1B1
rats.
conclusion,
our
results
suggested
KLF9,
epigenetic
silenced
DNMT1,
promoted
extracellular
signal‐regulated
kinase
(ERK)‐mediated
through
transcriptionally
regulating
CYP1B1.
Thus,
expected
new
target
for
treatment
OA.
