International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(17), P. 13336 - 13336
Published: Aug. 28, 2023
As
a
novel
form
of
regulated
cell
death,
ferroptosis
is
characterized
by
intracellular
iron
and
lipid
peroxide
accumulation,
which
different
from
other
death
forms
morphologically,
biochemically,
immunologically.
Ferroptosis
metabolism,
antioxidant
defense
systems
as
well
various
transcription
factors
related
signal
pathways.
Emerging
evidence
has
highlighted
that
associated
with
many
physiological
pathological
processes,
including
cancer,
neurodegeneration
diseases,
cardiovascular
ischemia/reperfusion
injury.
Noncoding
RNAs
are
group
functional
RNA
molecules
not
translated
into
proteins,
can
regulate
gene
expression
in
manners.
An
increasing
number
studies
have
shown
noncoding
RNAs,
especially
miRNAs,
lncRNAs,
circRNAs,
interfere
the
progression
modulating
ferroptosis-related
genes
or
proteins
directly
indirectly.
In
this
review,
we
summarize
basic
mechanisms
regulations
focus
on
recent
mechanism
for
types
ncRNAs
to
conditions,
will
deepen
our
understanding
regulation
provide
new
insights
employing
ferroptosis-associated
therapeutic
strategies.
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: Dec. 10, 2023
Abstract
Ferroptosis,
a
unique
modality
of
cell
death
with
mechanistic
and
morphological
differences
from
other
modes,
plays
pivotal
role
in
regulating
tumorigenesis
offers
new
opportunity
for
modulating
anticancer
drug
resistance.
Aberrant
epigenetic
modifications
posttranslational
(PTMs)
promote
resistance,
cancer
progression,
metastasis.
Accumulating
studies
indicate
that
can
transcriptionally
translationally
determine
vulnerability
to
ferroptosis
functions
as
driver
nervous
system
diseases
(NSDs),
cardiovascular
(CVDs),
liver
diseases,
lung
kidney
diseases.
In
this
review,
we
first
summarize
the
core
molecular
mechanisms
ferroptosis.
Then,
roles
processes,
including
histone
PTMs,
DNA
methylation,
noncoding
RNA
regulation
such
phosphorylation,
ubiquitination,
SUMOylation,
acetylation,
ADP-ribosylation,
are
concisely
discussed.
The
PTMs
genesis
cancers,
NSD,
CVDs,
well
application
PTM
modulators
therapy
these
then
discussed
detail.
Elucidating
mediated
by
will
facilitate
development
promising
combination
therapeutic
regimens
containing
or
PTM-targeting
agents
inducers
be
used
overcome
chemotherapeutic
resistance
could
prevent
addition,
highlight
potential
approaches
chemoresistance
halt
Biomedicine & Pharmacotherapy,
Journal Year:
2023,
Volume and Issue:
164, P. 114993 - 114993
Published: June 9, 2023
Cardiovascular
disease
(CVD)
is
a
major
contributor
to
increasing
morbidity
and
mortality
worldwide
seriously
threatens
human
health
life.
Cardiomyocyte
death
considered
the
pathological
basis
of
various
CVDs,
including
myocardial
infarction,
heart
failure,
aortic
dissection.
Multiple
mechanisms,
such
as
ferroptosis,
necrosis,
apoptosis,
contribute
cardiomyocyte
death.
Among
them,
ferroptosis
an
iron-dependent
form
programmed
cell
that
plays
vital
role
in
physiological
processes,
from
development
aging
immunity
CVD.
The
dysregulation
has
been
shown
be
closely
associated
with
CVD
progression,
yet
its
underlying
mechanisms
are
still
not
fully
understood.
In
recent
years,
growing
amount
evidence
suggests
non-coding
RNAs
(ncRNAs),
particularly
microRNAs,
long
RNAs,
circular
involved
regulation
thus
affecting
progression.
Some
ncRNAs
also
exhibit
potential
value
biomarker
and/or
therapeutic
target
for
patients
this
review,
we
systematically
summarize
findings
on
their
We
focus
clinical
applications
diagnostic
prognostic
biomarkers
well
targets
treatment.
DATA
AVAILABILITY:
No
new
data
were
created
or
analyzed
study.
Data
sharing
applicable
article.
Cell Biology and Toxicology,
Journal Year:
2024,
Volume and Issue:
40(1)
Published: March 21, 2024
Abstract
Cardiovascular
diseases
(CVDs)
are
the
main
that
endanger
human
health,
and
their
risk
factors
contribute
to
high
morbidity
a
rate
of
hospitalization.
Cell
death
is
most
important
pathophysiology
in
CVDs.
As
one
cell
mechanisms,
ferroptosis
new
form
regulated
(RCD)
broadly
participates
CVDs
(such
as
myocardial
infarction,
heart
transplantation,
atherosclerosis,
failure,
ischaemia/reperfusion
(I/R)
injury,
atrial
fibrillation,
cardiomyopathy
(radiation-induced
cardiomyopathy,
diabetes
sepsis-induced
cardiac
doxorubicin-induced
iron
overload
hypertrophic
cardiomyopathy),
pulmonary
arterial
hypertension),
involving
regulation,
metabolic
mechanism
lipid
peroxidation.
This
article
reviews
recent
research
on
regulation
its
relationship
with
occurrence
treatment
CVDs,
aiming
provide
ideas
targets
for
clinical
diagnosis
by
clarifying
latest
progress
research.
Graphical
•
The
identification,
development
history
characterization
ferroptosis.
role
different
subcellular
organelles
organelle-specific
regulators
includes
metabolism,
amino
acid
metabolism.
cardiovascular
cells
diseases.
efficacy
pathological
involved
Biomedicine & Pharmacotherapy,
Journal Year:
2021,
Volume and Issue:
141, P. 111872 - 111872
Published: July 7, 2021
Ferroptosis
is
a
type
of
regulated
cell
death
driven
by
iron
dependent
accumulation
cellular
reactive
oxygen
species
(ROS)
when
glutathione
(GSH)-dependent
lipid
peroxidation
repair
systems
are
compromised.
Nuclear
receptor
co-activator
4
(NCOA4)-mediated
selective
autophagy
ferritin,
termed
ferritinophagy,
involves
the
regulation
ferroptosis.
Emerging
evidence
has
revealed
that
ferritinophagy
and
ferroptosis
exert
significant
role
in
occurrence
development
cardiovascular
disease.
In
present
review,
we
aimed
to
brief
overview
focusing
on
underlying
mechanism
regulations
involved.
We
summarize
discuss
relevant
research
progress
diseases
accompanied
with
potential
applications
modulators
treatment
ferroptosis-associated
diseases.
Frontiers in Cardiovascular Medicine,
Journal Year:
2021,
Volume and Issue:
8
Published: July 22, 2021
Ferroptosis
is
an
iron-dependent
cell
death,
which
characterized
by
iron
overload
and
lipid
peroxidation.
distinct
from
apoptosis,
necroptosis,
autophagy,
other
types
of
death
in
morphology
function.
regulated
a
variety
factors
controlled
several
mechanisms,
including
mitochondrial
activity
metabolism
iron,
lipid,
amino
acids.
Accumulating
evidence
shows
that
ferroptosis
closely
related
to
majority
cardiovascular
diseases
(CVDs),
cardiomyopathy,
myocardial
infarction,
ischemia/reperfusion
injury,
heart
failure,
atherosclerosis.
This
review
summarizes
the
current
status
discusses
as
potential
therapeutic
target
for
CVDs.
Frontiers in Cell and Developmental Biology,
Journal Year:
2022,
Volume and Issue:
9
Published: Jan. 20, 2022
Ferroptosis
is
a
new
form
of
regulatory
cell
death
characterized
by
iron-dependent
and
intracellular
lipid
peroxidation.
can
be
divided
into
two
stages.
The
first
stage
iron
overload
in
the
cell,
which
generates
large
amount
reactive
oxygen
species
through
Fenton
reaction,
second
results
from
an
imbalance
antioxidant
system.
Excessive
phospholipid
hydroperoxides
cannot
removed
reduction
reactions,
as
this
could
destroy
membrane
structure
interfere
with
mitochondrial
function,
eventually
leading
to
ferroptosis
cell.
Cardiovascular
diseases
have
gradually
become
cause
modern
society.
relationship
between
occurrence
progression
cardiovascular
disease
has
research
hotspot
recent
years.
In
review,
we
summarize
mechanism
its
specific
role
disease.
Translational Lung Cancer Research,
Journal Year:
2022,
Volume and Issue:
11(3), P. 366 - 380
Published: March 1, 2022
Circular
ribonucleic
acids
(circRNAs)
play
a
key
role
in
the
development
of
different
types
cancer.
Ferroptosis
is
type
programmed
cell
death
that
contributes
to
cancer
progression.
However,
circRNAs
lung
adenocarcinoma
(LUAD)
ferroptosis
remains
unclear.The
gene
expression
levels
circRNA
P4HB
(circP4HB),
microRNA-1184
(miR-1184)
and
Solute
carrier
family
7
member
11
(Slc7a11),
also
known
as
Xct
were
detected
using
quantitative
real-time
polymerase
chain
reaction
(qRT-PCR).
established
LUAD
cells
was
induced
by
erastin.
Cell
viability
examined
via
Counting
Kit
8
assays.
evaluated
malondialdehyde
(MDA),
Prostaglandin-endoperoxide
Synthase
2
(Ptgs2),
lipid
reactive
oxygen
species
(lipid
ROS),
JC-1
detection.
The
mechanism
circP4HB/miR-1184/SLC7A11
investigated
luciferase
reporter
assays,
RNA
immunoprecipitation,
pull-down,
western
blot
A
functional
for
circP4HB
vivo
determined
xenograft
nude
mice
models.CircP4HB
increased
LUAD.
It
triggered
glutathione
(GSH)
synthesis
and,
therefore
protected
from
CircP4HB
may
function
competing
endogenous
modulating
miR-1184
regulate
SLC7A11.
inhibited
regulating
miR-1184/
SLC7A11-mediated
GSH
synthesis.
In
vivo,
overexpression
promoted
tumor
growth
ferroptosis.The
circRNA,
acts
novel
suppressor
Furthermore,
protects
modulation
miR-1184/SLC7A11
axis.
Our
findings
identified
biomarker
warrants
further
investigation
early
diagnosis
treatment
BMB Reports,
Journal Year:
2023,
Volume and Issue:
56(7), P. 416 - 416
Published: Jan. 27, 2023
Ovarian
cancer
(OC)
is
the
most
common
gynecological
malignancy
worldwide,
and
chemoresistance
occurs
in
patients,
resulting
treatment
failure.
A
better
understanding
of
molecular
processes
underlying
drug
resistance
crucial
for
development
efficient
therapies
to
improve
OC
patient
outcomes.
Circular
RNAs
(circRNAs)
ferroptosis
play
roles
tumorigenesis
chemotherapy.
However,
little
known
about
role(s)
circRNAs
regulating
OC.
To
gain
insights
into
cisplatin
OC,
we
studied
ferroptosis-associated
circRNA
circSnx12.
We
evaluated
circSnx12
expression
cell
lines
tissues
that
were
susceptible
or
resistant
using
quantitative
real-time
PCR.
also
conducted
vitro
vivo
assays
examining
function
mechanism
lnc-LBCSs.
Knockdown
rendered
cisplatin-resistant
cells
more
sensitive
by
activating
ferroptosis,
which
was
at
least
partially
abolished
downregulation
miR-194-5p.
Molecular
mechanics
studies
indicate
can
be
a
sponge
miR-194-5p,
targets
SLC7A11.
According
our
findings,
ameliorates
blocking
via
miR-194-5p/SLC7A11
pathway.
CircARNT2
may
thus
serve
as
an
effective
therapeutic
target
overcoming
[BMB
Reports
2023;
56(3):
184-189].