Frontiers in Physiology,
Journal Year:
2023,
Volume and Issue:
14
Published: Aug. 17, 2023
In
recent
years,
the
role
of
ferroptosis
in
pulmonary
fibrosis
has
garnered
increasing
interest
as
a
potential
therapeutic
target.
Pulmonary
is
pathological
process
characterized
by
accumulation
extracellular
matrix
affected
lung
tissues,
and
currently,
there
are
no
effective
therapies
for
preventing
or
reversing
fibrotic
lesions.
Ferroptosis
form
programmed
cell
death
that
regulated
network
enzymes
signaling
pathways.
Dysregulation
been
implicated
several
diseases,
including
fibrosis.
The
lipid
peroxides
course
causes
damage
to
membranes
other
cellular
components,
leading
ultimately
death.
Relevant
targets
intervention
include
key
enzymes,
such
glutathione
peroxidase
4,
transcription
factors
like
nuclear
factor
erythroid
2-related
2,
iron
chelation.
This
review
provides
an
overview
emerging
highlights
this
pathway.
Further
research
needed
develop
safe
approaches
targeting
treatment
Advanced Science,
Journal Year:
2024,
Volume and Issue:
unknown
Published: July 10, 2024
Abstract
Doxorubicin
(DOX)
is
an
effective
anticancer
agent,
but
its
clinical
utility
constrained
by
dose‐dependent
cardiotoxicity,
partly
due
to
cardiomyocyte
ferroptosis.
However,
the
progress
of
developing
cardioprotective
medications
counteract
ferroptosis
has
encountered
obstacles.
Protosappanin
A
(PrA),
anti‐inflammatory
compound
derived
from
hematoxylin,
shows
potential
against
DOX‐induced
cardiomyopathy
(DIC).
Here,
it
reported
that
PrA
alleviates
myocardial
damage
and
dysfunction
reducing
maintaining
mitochondrial
homeostasis.
Subsequently,
molecular
target
through
proteome
microarray,
docking,
dynamics
simulation
identified.
Mechanistically,
physically
binds
with
ferroptosis‐related
proteins
acyl‐CoA
synthetase
long‐chain
family
member
4
(ACSL4)
ferritin
heavy
chain
1
(FTH1),
ultimately
inhibiting
ACSL4
phosphorylation
subsequent
phospholipid
peroxidation,
while
also
preventing
FTH1
autophagic
degradation
release
ferrous
ions
(Fe
2+
)
release.
Given
critical
role
in
pathogenesis
ischemia‐reperfusion
(IR)
injury,
this
further
investigation
posits
can
confer
a
protective
effect
IR‐induced
cardiac
Overall,
novel
pharmacological
inhibitor
unveiled
targets
uncover
dual‐regulated
mechanism
for
DIC,
highlighting
additional
therapeutic
options
chemodrug‐induced
cardiotoxicity
ferroptosis‐triggered
disorders.
Redox Biology,
Journal Year:
2024,
Volume and Issue:
72, P. 103158 - 103158
Published: April 12, 2024
Exposure
to
PM2.5
is
correlated
with
cardiac
remodeling,
of
which
hypertrophy
one
the
main
clinical
manifestations.
Ferroptosis
plays
an
important
role
in
hypertrophy.
However,
potential
mechanism
PM2.5-induced
through
ferroptosis
remains
unclear.
This
study
aimed
explore
molecular
caused
by
and
intervention
MitoQ
involved
this
process.
The
results
showed
that
could
induce
dysfunction
mice.
Meanwhile,
characteristics
were
observed,
such
as
iron
homeostasis
imbalance,
lipid
peroxidation,
mitochondrial
damage
abnormal
expression
key
molecules.
treatment
effectively
mitigate
these
alternations.
After
treating
human
cardiomyocyte
AC16
PM2.5,
activator
(Erastin)
inhibitor
(Fer-1),
it
was
found
promote
ferritinophagy
lead
well
accumulation
intracellular
labile
iron.
Subsequently,
mitophagy
activated
provided
additional
source
iron,
enhancing
sensitivity
cells
ferroptosis.
Furthermore,
Fer-1
alleviated
cytotoxicity
overload
cytoplasm
mitochondria
cells.
It
worth
noting
during
process
ferroptosis,
metabolism
mediated
activation
a
temporal
order.
In
addition,
NCOA4
knockdown
reversed
imbalance
peroxidation
thereby
alleviating
summary,
our
imbalance-mediated
crosstalk
played
Redox Biology,
Journal Year:
2024,
Volume and Issue:
71, P. 103100 - 103100
Published: March 8, 2024
Th2-high
asthma
is
characterized
by
elevated
levels
of
type
2
cytokines,
such
as
interleukin
13
(IL-13),
and
its
prevalence
has
been
increasing
worldwide.
Ferroptosis,
a
recently
discovered
programmed
cell
death,
involved
in
the
pathological
process
asthma;
however,
underlying
mechanisms
remain
incompletely
understood.
In
this
study,
we
demonstrated
that
serum
level
malondialdehyde
(MDA),
an
index
lipid
peroxidation,
positively
correlated
with
IL-13
negatively
predicted
forced
expiratory
volume
1
s
(FEV1%)
asthmatics.
Furthermore,
showed
facilitates
ferroptosis
upregulating
suppressor
cytokine
signaling
(SOCS1)
through
analyzing
immortalized
airway
epithelial
cells,
human
organoids,
ovalbumin
(OVA)-challenged
model.
We
identified
signal
transducer
activator
transcription
6
(STAT6)
promotes
SOCS1
upon
stimulation.
Moreover,
SOCS1,
E3
ubiquitin
ligase,
was
found
to
bind
solute
carrier
family
7
member
11
(SLC7A11)
catalyze
ubiquitinated
degradation,
thereby
promoting
cells.
Last,
inhibiting
can
decrease
cells
alleviate
hyperresponsiveness
(AHR)
OVA-challenged
wide-type
mice,
while
overexpression
exacerbated
above
IL-13-knockout
mice.
Our
findings
reveal
IL-13/STAT6/SOCS1/SLC7A11
pathway
novel
molecular
mechanism
for
asthma,
confirming
targeting
potential
therapeutic
strategy
asthma.
Phytomedicine,
Journal Year:
2024,
Volume and Issue:
130, P. 155738 - 155738
Published: June 1, 2024
Respiratory
diseases
pose
a
grave
threat
to
human
life.
Therefore,
understanding
their
pathogenesis
and
therapeutic
strategy
is
important.
Ferroptosis
novel
type
of
iron-dependent
programmed
cell
death,
distinct
from
apoptosis,
necroptosis,
autophagy,
characterised
by
iron,
reactive
oxygen
species,
lipid
peroxide
accumulation,
as
well
glutathione
(GSH)
depletion
GSH
peroxidase
4
(GPX4)
inactivation.
A
close
association
between
ferroptosis
the
onset
progression
respiratory
diseases,
including
chronic
obstructive
pulmonary
disease,
acute
lung
injury,
bronchial
asthma,
fibrosis,
cancer,
has
been
reported.
Recent
studies
have
shown
that
traditional
Chinese
medicine
(TCM)
compounds
exhibit
unique
advantages
in
treatment
owing
natural
properties
potential
efficacy.
These
can
effectively
regulate
modulating
several
key
signalling
pathways
such
system
Xc
Ecotoxicology and Environmental Safety,
Journal Year:
2024,
Volume and Issue:
277, P. 116314 - 116314
Published: April 19, 2024
Fine
particulate
matter
(PM2.5)
has
been
extensively
implicated
in
the
pathogenesis
of
neurodevelopmental
disorders,
but
underlying
mechanism
remains
unclear.
Recent
studies
have
revealed
that
PM2.5
plays
a
role
regulating
iron
metabolism
and
redox
homeostasis
brain,
which
is
closely
associated
with
ferroptosis.
In
this
study,
ferroptosis
PM2.5-induced
neurotoxicity
were
investigated
mice,
primary
hippocampal
neurons,
HT22
cells.
Our
findings
demonstrated
exposure
to
could
induce
abnormal
behaviors,
neuroinflammation,
neuronal
loss
hippocampus
mice.
These
effects
may
be
attributed
induced
by
neurons.
RNA-seq
analysis
upregulation
metabolism-related
protein
Heme
Oxygenase
1
(HO-1)
activation
mitophagy
might
play
key
roles
Subsequent
vitro
experiments
showed
significantly
upregulated
HO-1
neurons
Moreover,
activated
cells,
leading
mitochondrial
membrane
potential,
alterations
expression
autophagy-related
proteins
LC3,
P62,
mTOR,
as
well
an
increase
mitophagy-related
PINK1
PARKIN.
As
heme-degradation
enzyme,
promotes
release
excess
iron,
genetically
inhibiting
cells
prevent
both
Furthermore,
pharmacological
inhibition
reduced
levels
ferrous
ions
lipid
peroxides,
thereby
preventing
Collectively,
study
demonstrates
mediates
mitophagy-dependent
or
therapeutic
target
ameliorate
following
exposure.
