International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(2), P. 897 - 897
Published: Jan. 11, 2024
The
hospital
mortality
in
patients
with
ST-segment
elevation
myocardial
infarction
(STEMI)
is
about
6%
and
has
not
decreased
recent
years.
leading
cause
of
death
these
ischemia/reperfusion
(I/R)
cardiac
injury.
It
quite
obvious
that
there
an
urgent
need
to
create
new
drugs
for
the
treatment
STEMI
based
on
knowledge
pathogenesis
I/R
injury,
particular,
molecular
mechanism
ferroptosis.
In
this
study,
it
was
demonstrated
ferroptosis
involved
development
antitumor
drug-induced
cardiomyopathy,
diabetic
septic
inflammation.
There
indirect
evidence
participates
stress-induced
activation
AMPK,
PKC,
ERK1/2,
PI3K,
Akt
prevents
inhibition
HO-1
alleviates
roles
GSK-3β
NOS
regulation
require
further
study.
stimulation
Nrf2,
STAT3
TLR4
NF-κB
promotes
cardiomyocytes.
MiR-450b-5p
miR-210-3p
can
increase
tolerance
cardiomyocytes
hypoxia/reoxygenation
through
Circ_0091761
RNA,
miR-214-3p,
miR-199a-5p,
miR-208a/b,
miR-375-3p,
miR-26b-5p
miR-15a-5p
aggravate
Biomedicine & Pharmacotherapy,
Journal Year:
2023,
Volume and Issue:
170, P. 116057 - 116057
Published: Dec. 29, 2023
In
the
21st
century,
cardiovascular
disease
(CVD)
has
become
one
of
leading
causes
death
worldwide.
The
prevention
and
treatment
CVD
remain
pressing
scientific
issues.
Several
recent
studies
have
suggested
that
ferroptosis
may
play
a
key
role
in
CVD.
Most
conducted
thus
far
on
supported
link.
Ferroptosis
mediated
by
different
signaling
metabolic
pathways
can
lead
to
ischemic
heart
disease,
myocarditis,
failure,
ischemia-reperfusion
injury,
cardiomyopathy.
Still,
specific
mechanism
CVD,
particular
organ
areas
affected,
stage
involved
need
be
further
studied.
Therefore,
understanding
mechanisms
regulating
improve
management.
Throughout
this
review,
we
summarized
its
effect
pathogenesis
We
also
predicted
discussed
future
research
directions,
aiming
provide
new
ideas
strategies
for
preventing
treating
Life Sciences,
Journal Year:
2024,
Volume and Issue:
340, P. 122439 - 122439
Published: Jan. 24, 2024
Myocardial
ischemia–reperfusion
injury
(MIRI),
caused
by
the
initial
interruption
and
subsequent
restoration
of
coronary
artery
blood,
results
in
further
damage
to
cardiac
function,
affecting
prognosis
patients
with
acute
myocardial
infarction.
Ferroptosis
is
an
iron-dependent,
superoxide-driven,
non-apoptotic
form
regulated
cell
death
that
involved
pathogenesis
MIRI.
characterized
accumulation
lipid
peroxides
(LOOH)
redox
disequilibrium.
Free
iron
ions
can
induce
oxidative
stress
as
a
substrate
Fenton
reaction
lipoxygenase
(LOX)
participate
inactivation
variety
antioxidants
including
CoQ10
GPX4,
destroying
balance
causing
death.
The
metabolism
amino
acid,
iron,
lipids,
associated
pathways,
considered
specific
hallmark
ferroptosis.
This
review
systematically
summarizes
latest
research
progress
on
mechanisms
ferroptosis
discusses
analyzes
therapeutic
approaches
targeting
alleviate
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(2), P. 897 - 897
Published: Jan. 11, 2024
The
hospital
mortality
in
patients
with
ST-segment
elevation
myocardial
infarction
(STEMI)
is
about
6%
and
has
not
decreased
recent
years.
leading
cause
of
death
these
ischemia/reperfusion
(I/R)
cardiac
injury.
It
quite
obvious
that
there
an
urgent
need
to
create
new
drugs
for
the
treatment
STEMI
based
on
knowledge
pathogenesis
I/R
injury,
particular,
molecular
mechanism
ferroptosis.
In
this
study,
it
was
demonstrated
ferroptosis
involved
development
antitumor
drug-induced
cardiomyopathy,
diabetic
septic
inflammation.
There
indirect
evidence
participates
stress-induced
activation
AMPK,
PKC,
ERK1/2,
PI3K,
Akt
prevents
inhibition
HO-1
alleviates
roles
GSK-3β
NOS
regulation
require
further
study.
stimulation
Nrf2,
STAT3
TLR4
NF-κB
promotes
cardiomyocytes.
MiR-450b-5p
miR-210-3p
can
increase
tolerance
cardiomyocytes
hypoxia/reoxygenation
through
Circ_0091761
RNA,
miR-214-3p,
miR-199a-5p,
miR-208a/b,
miR-375-3p,
miR-26b-5p
miR-15a-5p
aggravate
