Drug Design Development and Therapy,
Год журнала:
2024,
Номер
Volume 18, С. 6115 - 6132
Опубликована: Дек. 1, 2024
Ciprofol
is
a
novel
intravenous
anesthetic
that
has
been
increasingly
used
in
clinical
anesthesia
and
sedation.
Studies
suggested
ciprofol
reduced
oxidative
stress
inflammatory
responses
to
alleviate
cerebral
ischemia/reperfusion
(I/R)
injury,
but
whether
protects
the
heart
against
I/R
injury
mechanisms
are
unknown.
Herein,
we
assessed
effects
of
on
ferroptosis
during
myocardial
injury.
Signal Transduction and Targeted Therapy,
Год журнала:
2024,
Номер
9(1)
Опубликована: Окт. 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 Translational Medicine,
Год журнала:
2025,
Номер
23(1)
Опубликована: Апрель 10, 2025
Acute
myocardial
infarction
(AMI)
and
the
ischemia-reperfusion
injury
(MI/RI)
that
typically
ensues
represent
a
significant
global
health
burden,
accounting
for
considerable
number
of
deaths
disabilities.
In
context
AMI,
percutaneous
coronary
intervention
(PCI)
is
preferred
treatment
option
reducing
acute
ischemic
damage
to
heart.
Despite
modernity
PCI
therapy,
pathological
cardiomyocytes
due
MI/RI
remains
an
important
target
affects
long-term
prognosis
patients.
recent
years,
mitochondrial
dysfunction
during
AMI
has
been
increasingly
recognized
as
critical
factor
in
cardiomyocyte
death.
Damaged
mitochondria
play
active
role
formation
inflammatory
environment
by
triggering
key
signaling
pathways,
including
those
mediated
cyclic
GMP-AMP
synthase,
NOD-like
receptors
Toll-like
receptors.
This
review
emphasizes
dual
both
contributors
regulators
inflammation.
The
aim
explore
complex
mechanisms
its
profound
impact
on
immune
dysregulation.
Specific
interventions
mitochondrial-targeted
antioxidants,
membrane-stabilizing
peptides,
transplantation
therapies
have
demonstrated
efficacy
preclinical
models.
Food & Function,
Год журнала:
2023,
Номер
14(22), С. 10052 - 10068
Опубликована: Янв. 1, 2023
Background:
Myocardial
ischemia
and
reperfusion
injury
(MIRI)
is
a
severe
complication
of
revascularization
therapy
in
patients
with
myocardial
infarction.
Therefore,
there
an
urgent
requirement
to
find
more
therapeutic
solutions
for
MIRI.
Recently,
ferroptosis,
which
characterized
by
lipid
peroxidation,
was
considered
critical
contributor
Fucoxanthin
(FX),
natural
antioxidant
carotenoid,
abundant
brown
seaweed,
exerts
protective
effects
under
various
pathological
conditions.
However,
whether
FX
alleviates
MIRI
unclear.
This
study
aims
clarify
the
on
Methods:
Mice
left
anterior
descending
artery
ligation
were
used
as
vivo
models.
Neonatal
rat
cardiomyocytes
(NRCs)
induced
hypoxia
vitro
TTC-Evans
blue
staining
performed
validate
infarction
size.
Transmission
electron
microscopy
employed
detect
mitochondrial
cardiomyocytes.
In
addition,
4
weeks
after
MIRI,
echocardiography
measure
cardiac
function;
fluorescent
probes
western
blots
ferroptosis.
Results:
showed
that
reduced
size
ameliorated
MIRI-induced
myofibril
loss
mitochondrion
shrinkage.
Furthermore,
improved
LVEF
LVFS
inhibited
hypertrophy
fibrosis
mice
study,
calcein
AM/PI
TUNEL
cell
death
caused
treatment.
DCFH-DA
MitoSOX
indicated
cellular
reactive
oxygen
species
(ROS).
Moreover,
C11-BODIPY
581/591
staining,
ferro-orange
MDA
assay,
Fe2+
4-hydroxynonenal
enzyme-linked
immunosorbent
blot
results
revealed
ferroptosis
vivo,
inhibiting
ROS
release,
well
modulating
hallmark
FTH,
TFRC,
GPX4
expression.
Additionally,
eliminated
NRF2
inhibitor
brusatol,
observed
from
blotting,
indicating
exerted
cardio-protective
through
pathway.
Conclusion:
Our
alleviated
inhibition
via
signaling
Scientific Reports,
Год журнала:
2023,
Номер
13(1)
Опубликована: Окт. 18, 2023
Abstract
Increasing
evidences
demonstrate
that
chlorogenic
acid
(CGA),
a
polyphenol
with
multiple
effects
such
as
anti-inflammatory
and
anti-oxidation,
protects
against
myocardial
ischemia–reperfusion
injury
(MIRI)
in
vitro
vivo.
But
its
detailed
cardiac
protection
mechanism
is
still
unclear.
The
MIRI
mice
model
was
established
by
ligating
the
left
anterior
descending
branch
(LAD)
of
coronary
artery
C57BL/6
mice.
Sixty
were
randomly
divided
into
four
groups.
CGA
group
+
I/R
(each
n
=
15)
gavaged
30
mg/kg/day
for
4
weeks.
Sham
administered
equal
volumes
saline.
In
constructed
hypoxia
reoxygenation
HL-1
cardiomyocytes.
results
showed
pretreatment
reduced
infarction
size
cTnT
contents
serum,
simultaneously
levels
Lnc
Neat1
expression
attenuated
NLRP3
inflammasome-mediated
pyroptosis
tissue.
Consistent
vivo
results,
0.2
μM
2
12
h
cardiomyocytes
depressed
hypoxia/reoxygenation-induced
expression,
inflammasome
activation
pyroptosis.
shRNA
transfection
mediated
lentivirus
significantly
Our
findings
suggest
depressing
pyrotosis.
Inhibiting
may
be
therapeutic
strategy
MIRI.
Biomedicine & Pharmacotherapy,
Год журнала:
2024,
Номер
174, С. 116542 - 116542
Опубликована: Апрель 3, 2024
Previous
studies
have
demonstrated
that
the
underlying
mechanisms
of
myocardial
ischemia/reperfusion
injury
(MIRI)
are
complex
and
involve
multiple
types
regulatory
cell
death,
including
ferroptosis,
apoptosis,
autophagy.
Thus,
we
aimed
to
identify
MIRI
validate
protective
role
epigallocatechin-3-gallate
(EGCG)
its
related
in
MIRI.
An
vivo
vitro
models
were
constructed.
The
results
showed
pretreatment
with
EGCG
could
attenuate
MIRI,
as
indicated
by
increased
viability,
reduced
lactate
dehydrogenase
(LDH)
activity
inhibited
iron
overload,
abnormal
lipid
metabolism,
preserved
mitochondrial
function,
decreased
infarct
size,
maintained
cardiac
reactive
oxygen
species
(ROS)
level,
TUNEL-positive
cells.
Additionally,
autophagy
induced
via
upregulating
14–3–3η
protein
levels.
Furthermore,
effects
be
abolished
pAd/14–3–3η-shRNA
or
Compound
C11
(a
inhibitor)
but
not
pAd/NC-shRNA.
In
conclusion,
attenuated
mediating
protected
cardiomyocytes
against
Frontiers in Pharmacology,
Год журнала:
2024,
Номер
15
Опубликована: Окт. 1, 2024
Myocardial
ischemia-reperfusion
injury
(MIRI)
is
a
significant
factor
in
the
development
of
cardiac
dysfunction
following
myocardial
infarction.
Ferroptosis,
type
regulated
cell
death
driven
by
iron
and
marked
lipid
peroxidation,
has
garnered
growing
interest
for
its
crucial
involvement
pathogenesis
MIRI.This
review
comprehensively
examines
mechanisms
ferroptosis,
focusing
on
regulation
through
metabolism,
VDAC
signaling,
antioxidant
system
dysregulation.
We
also
compare
ferroptosis
with
other
forms
to
highlight
distinct
characteristics.
Furthermore,
MIRI
examined
focus
recent
discoveries
concerning
ROS
generation,
mitochondrial
impairment,
autophagic
processes,
ER
stress,
non-coding
RNA
regulation.
Lastly,
emerging
therapeutic
strategies
that
inhibit
mitigate
are
reviewed,
providing
new
insights
into
potential
clinical
applications.
Frontiers in Bioengineering and Biotechnology,
Год журнала:
2024,
Номер
12
Опубликована: Авг. 15, 2024
Heart
failure
is
a
major
health
problem
in
which
the
heart
unable
to
pump
enough
blood
meet
body’s
needs.
It
progressive
disease
that
becomes
more
severe
over
time
and
can
be
caused
by
variety
of
factors,
including
attack,
cardiomyopathy
valve
disease.
There
are
various
methods
cure
this
disease,
has
many
complications
risks.
The
advancement
knowledge
technology
proposed
new
for
diseases.
One
promising
treatments
tissue
engineering.
Tissue
engineering
field
research
aims
create
living
tissues
organs
replace
damaged
or
diseased
tissue.
goal
improve
cardiac
function
reduce
need
transplantation.
This
done
using
three
important
principles
cells,
biomaterials
signals
techniques
cells
such
as
electrospinning,
hydrogel
synthesis,
decellularization,
etc.
diverse.
Treating
through
still
under
development
research,
but
it
hoped
there
will
no
transplants
invasive
surgeries
near
future.
In
study,
based
on
most
recent
years,
we
examine
power
treatment
failure.
