Journal of Lipid Research,
Год журнала:
2024,
Номер
65(2), С. 100499 - 100499
Опубликована: Янв. 11, 2024
Ferroptosis
is
a
novel
cell
death
mechanism
that
mediated
by
iron-dependent
lipid
peroxidation.
It
may
be
involved
in
atherosclerosis
development.
Products
of
phospholipid
oxidation
play
key
role
atherosclerosis.
1-palmitoyl-2-glutaroyl-sn-glycero-3-phosphocholine
(PGPC)
product
present
atherosclerotic
lesions.
remains
unclear
whether
PGPC
causes
inducing
endothelial
ferroptosis.
In
this
study,
human
umbilical
vein
cells
(HUVECs)
were
treated
with
PGPC.
Intracellular
levels
ferrous
iron,
peroxidation,
superoxide
anions
(O2•-),
and
glutathione
detected,
expression
fatty
acid
binding
protein-3
(FABP3),
peroxidase
4
(GPX4),
CD36
measured.
Additionally,
the
mitochondrial
membrane
potential
(MMP)
was
determined.
Aortas
from
C57BL6
mice
isolated
for
vasodilation
testing.
Results
showed
increased
iron
levels,
production
peroxidation
O2•-,
FABP3
expression.
However,
inhibited
GPX4
destroyed
normal
MMP.
These
effects
also
blocked
ferrostatin-1,
an
inhibitor
silencing
significantly
reversed
effect
Furthermore,
stimulated
Conversely,
PGPC,
including
PGPC-induced
Importantly,
E06,
direct
oxidized
1-palmitoyl-2-arachidonoyl-phosphatidylcholine
IgM
natural
antibody,
Finally,
impaired
endothelium-dependent
vasodilation,
ferrostatin-1
or
inhibitors
impairment.
Our
data
demonstrate
impairs
function
ferroptosis
through
receptor
to
increase
findings
provide
new
insights
into
mechanisms
therapeutic
target
Antioxidants,
Год журнала:
2022,
Номер
11(3), С. 555 - 555
Опубликована: Март 15, 2022
The
heme
oxygenase
(HO)
enzyme
system
catabolizes
to
carbon
monoxide
(CO),
ferrous
iron,
and
biliverdin-IXα
(BV),
which
is
reduced
bilirubin-IXα
(BR)
by
biliverdin
reductase
(BVR).
HO
activity
represented
two
distinct
isozymes,
the
inducible
form,
HO-1,
a
constitutive
HO-2,
encoded
genes
(HMOX1,
HMOX2,
respectively).
HO-1
responds
transcriptional
activation
in
response
wide
variety
of
chemical
physical
stimuli,
including
its
natural
substrate
heme,
oxidants,
phytochemical
antioxidants.
expression
regulated
NF-E2-related
factor-2
counter-regulated
Bach-1,
heme-sensitive
manner.
Additionally,
HMOX1
promoter
polymorphisms
have
been
associated
with
human
disease.
induction
can
confer
protection
inflammatory
conditions
through
removal
pro-oxidant
potential
catalyst
lipid
peroxidation,
whereas
iron
released
from
may
trigger
ferritin
synthesis
or
ferroptosis.
production
heme-derived
reaction
products
(i.e.,
BV,
BR)
contribute
HO-dependent
cytoprotection
via
antioxidant
immunomodulatory
effects.
BVR
BR
newly
recognized
roles
regulation.
CO
alter
mitochondrial
function
leading
modulation
downstream
signaling
pathways
that
culminate
anti-apoptotic,
anti-inflammatory,
anti-proliferative
This
review
will
present
evidence
for
beneficial
effects
diseases,
cardiovascular
disease
(CVD),
metabolic
conditions,
diabetes
obesity,
as
well
acute
chronic
diseases
liver,
kidney,
lung.
Strategies
targeting
pathway,
genetic
expression,
application
BR,
gas,
donor
compounds
show
therapeutic
organ
ischemia/reperfusion
injury.
Evidence
studies
indicate
represent
biomarker
oxidative
stress
various
clinical
while
increases
serum
levels
correlated
inversely
risk
CVD
Ongoing
trials
investigate
Frontiers in Cell and Developmental Biology,
Год журнала:
2022,
Номер
9
Опубликована: Янв. 13, 2022
Atherosclerosis
is
a
chronic
inflammatory
disorder
characterized
by
the
gradual
buildup
of
plaques
within
vessel
wall
middle-sized
and
large
arteries.
The
occurrence
development
atherosclerosis
rupture
are
related
to
injury
vascular
cells,
including
endothelial
smooth
muscle
macrophages.
Autophagy
subcellular
process
that
plays
an
important
role
in
degradation
proteins
damaged
organelles,
autophagy
cells
closely
atherosclerosis.
Pyroptosis
proinflammatory
form
regulated
cell
death,
while
ferroptosis
nonapoptotic
death
involving
overwhelming
iron-dependent
lipid
peroxidation.
Both
them
exhibit
distinct
features
from
apoptosis,
necrosis,
morphology,
biochemistry,
genetics.
However,
growing
body
evidence
suggests
pyroptosis
interact
with
participate
cancers,
degenerative
brain
diseases
cardiovascular
diseases.
This
review
updated
current
understanding
autophagy,
pyroptosis,
ferroptosis,
finding
potential
links
their
effects
on
atherogenesis
plaque
stability,
thus
providing
ways
develop
new
pharmacological
strategies
address
stabilize
vulnerable,
ruptured
plaques.
Molecular Metabolism,
Год журнала:
2022,
Номер
60, С. 101470 - 101470
Опубликована: Март 15, 2022
With
long-term
metabolic
malfunction,
diabetes
can
cause
serious
damage
to
whole-body
tissue
and
organs,
resulting
in
a
variety
of
complications.
Therefore,
it
is
particularly
important
further
explore
the
pathogenesis
complications
develop
drugs
for
prevention
treatment.
In
recent
years,
different
from
apoptosis
necrosis,
ferroptosis
has
been
recognized
as
new
regulatory
mode
cell
death
involves
regulation
nuclear
receptor
coactivator
4
(NCOA4)-mediated
ferritinophagy.
Evidence
shows
that
ferritinophagy
play
significant
role
occurrence
development
Frontiers in Endocrinology,
Год журнала:
2022,
Номер
13
Опубликована: Март 29, 2022
The
global
diabetes
epidemic
and
its
complications
are
increasing,
thereby
posing
a
major
threat
to
public
health.
A
comprehensive
understanding
of
mellitus
(DM)
is
necessary
for
the
development
effective
treatments.
Ferroptosis
newly
identified
form
programmed
cell
death
caused
by
production
reactive
oxygen
species
an
imbalance
in
iron
homeostasis.
Increasing
evidence
suggests
that
ferroptosis
plays
pivotal
role
pathogenesis
diabetes-related
complications.
In
this
review,
we
summarize
potential
impact
regulatory
mechanisms
on
complications,
as
well
inhibitors
diabetic
Therefore,
developing
drugs
or
agents
target
may
provide
new
treatment
strategies
patients
with
diabetes.
Nutrients,
Год журнала:
2023,
Номер
15(3), С. 591 - 591
Опубликована: Янв. 23, 2023
Iron
functions
as
an
essential
micronutrient
and
participates
in
normal
physiological
biochemical
processes
the
cardiovascular
system.
Ferroptosis
is
a
novel
type
of
iron-dependent
cell
death
driven
by
iron
accumulation
lipid
peroxidation,
characterized
depletion
glutathione
suppression
peroxidase
4
(GPX4).
Dysregulation
metabolism
ferroptosis
have
been
implicated
occurrence
development
diseases
(CVDs),
including
hypertension,
atherosclerosis,
pulmonary
myocardial
ischemia/reperfusion
injury,
cardiomyopathy,
heart
failure.
chelators
deferoxamine
dexrazoxane,
lipophilic
antioxidants
ferrostatin-1
liproxstatin-1
revealed
to
abolish
suppress
peroxidation
other
CVDs.
Notably,
inhibition
has
demonstrated
alleviate
cardiac
impairments,
fibrosis
pathological
remodeling
during
hypertension
potentiating
GPX4
signaling.
Administration
improved
injury
inhibiting
peroxidation.
Several
small
molecules
may
be
effective
treatment
ferroptosis-mediated
In
this
article,
we
summarize
regulatory
roles
underlying
mechanisms
dysregulation
Targeting
are
potential
therapeutic
strategies
prevention
Experimental Hematology and Oncology,
Год журнала:
2023,
Номер
12(1)
Опубликована: Июль 27, 2023
Abstract
Background
Ferroptosis
is
a
regulated
cell
death
mode
triggered
by
iron-dependent
toxic
membrane
lipid
peroxidation.
As
novel
modality
that
morphologically
and
mechanistically
different
from
other
forms
of
death,
such
as
apoptosis
necrosis,
ferroptosis
has
attracted
extensive
attention
due
to
its
association
with
various
diseases.
Evidence
on
potential
therapeutic
strategy
accumulated
the
rapid
growth
research
targeting
for
tumor
suppression
in
recent
years.
Methods
We
summarize
currently
known
characteristics
major
regulatory
mechanisms
present
role
cellular
stress
responses,
including
ER
autophagy.
Furthermore,
we
elucidate
applications
radiotherapy
immunotherapy,
which
will
be
beneficial
exploring
new
strategies
clinical
treatment.
Result
conclusion
Based
specific
biomarkers
precise
patient-specific
assessment,
great
translated
into
practical
approaches
cancer
therapy,
significantly
contributing
prevention,
diagnosis,
prognosis,
treatment
cancer.
Frontiers in Endocrinology,
Год журнала:
2024,
Номер
15
Опубликована: Апрель 5, 2024
Diabetic
vascular
complications
are
prevalent
and
severe
among
diabetic
patients,
profoundly
affecting
both
their
quality
of
life
long-term
prospects.
These
can
be
classified
into
macrovascular
microvascular
complications.
Under
the
impact
risk
factors
such
as
elevated
blood
glucose,
pressure,
cholesterol
lipids,
endothelium
undergoes
endothelial
dysfunction,
characterized
by
increased
inflammation
oxidative
stress,
decreased
NO
biosynthesis,
endothelial-mesenchymal
transition,
senescence,
even
cell
death.
processes
will
ultimately
lead
to
diseases,
with
diseases
mainly
atherosclerosis
(AS)
thickening
basement
membrane.
It
further
indicates
a
primary
contributor
morbidity
mortality
observed
in
individuals
diabetes.
In
this
review,
we
delve
intricate
mechanisms
that
drive
dysfunction
during
diabetes
progression
its
associated
Furthermore,
outline
various
pharmacotherapies
targeting
hope
accelerating
effective
therapeutic
drug
discovery
for
early
control
