Cell Death and Disease,
Journal Year:
2022,
Volume and Issue:
13(5)
Published: May 18, 2022
The
concept
of
cell
death
has
been
expanded
beyond
apoptosis
and
necrosis
to
additional
forms,
including
necroptosis,
pyroptosis,
autophagy,
ferroptosis.
These
modalities
play
a
critical
role
in
all
aspects
life,
which
are
noteworthy
for
their
diverse
roles
diseases.
Atherosclerosis
(AS)
vascular
calcification
(VC)
major
causes
the
high
morbidity
mortality
cardiovascular
disease.
Despite
considerable
advances
understanding
signaling
pathways
associated
with
AS
VC,
exact
molecular
basis
remains
obscure.
In
article,
we
review
mechanisms
that
mediate
its
implications
VC.
A
better
underlying
VC
may
drive
development
promising
therapeutic
strategies.
Theranostics,
Journal Year:
2021,
Volume and Issue:
11(7), P. 3052 - 3059
Published: Jan. 1, 2021
Cell
death
is
an
important
component
of
the
pathophysiology
cardiovascular
disease.
An
understanding
how
cardiomyocytes
die,
and
why
regeneration
cells
in
heart
limited,
a
critical
area
study.
Ferroptosis
form
regulated
cell
that
characterized
by
iron
overload,
leading
to
accumulation
lethal
levels
lipid
hydroperoxides.
The
metabolism
iron,
lipids,
amino
acids
glutathione
tightly
controls
initiation
execution
ferroptosis.
Emerging
evidence
shows
ferroptosis
closely
associated
with
occurrence
progression
various
diseases.
In
recent
years,
has
been
found
play
roles
cardiomyopathy,
myocardial
infarction,
ischemia/reperfusion
injury,
failure.
This
article
reviews
mechanisms
which
initiated
controlled
discusses
as
novel
therapeutic
target
for
Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
13
Published: Nov. 1, 2022
The
endothelium
is
a
single
layer
of
epithelium
covering
the
surface
vascular
system,
and
it
represents
physical
barrier
between
blood
vessel
wall
that
plays
an
important
role
in
maintaining
intravascular
homeostasis.
However,
endothelial
dysfunction
or
cell
death
can
cause
disruption,
vasoconstriction
diastolic
dysfunction,
smooth
muscle
proliferation
migration,
inflammatory
responses,
thrombosis,
which
are
closely
associated
with
progression
several
diseases,
such
as
atherosclerosis,
hypertension,
coronary
atherosclerotic
heart
disease,
ischemic
stroke,
acute
lung
injury,
kidney
diabetic
retinopathy,
Alzheimer’s
disease.
Oxidative
stress
caused
by
overproduction
reactive
oxygen
species
(ROS)
mechanism
underlying
death.
Growing
evidence
suggests
ROS
trigger
various
ways,
including
pyroptosis,
parthanatos,
ferroptosis.
Therefore,
this
review
will
systematically
illustrate
source
cells
(ECs);
reveal
molecular
ferroptosis
ECs;
provide
new
ideas
for
research
treatment
dysfunction-related
diseases.
Acta Pharmaceutica Sinica B,
Journal Year:
2020,
Volume and Issue:
10(10), P. 1866 - 1879
Published: April 9, 2020
Mitochondrial
damage
is
a
critical
contributor
to
cardiac
ischemia/reperfusion
(I/R)
injury.
quality
control
(MQC)
mechanisms,
series
of
adaptive
responses
that
preserve
mitochondrial
structure
and
function,
ensure
cardiomyocyte
survival
function
after
I/R
MQC
includes
fission,
fusion,
mitophagy
mitochondria-dependent
cell
death.
The
interplay
among
these
linked
pathological
changes
such
as
redox
imbalance,
calcium
overload,
energy
metabolism
disorder,
signal
transduction
arrest,
the
unfolded
protein
response
endoplasmic
reticulum
stress.
Excessive
fission
an
early
marker
Reduced
fusion
has
been
observed
in
stressed
cardiomyocytes
correlates
with
dysfunction
depression.
Mitophagy
allows
autophagosomes
selectively
degrade
poorly
structured
mitochondria,
thus
maintaining
network
fitness.
Nevertheless,
abnormal
maladaptive
Although
mitochondria
serve
fuel
source
heart
by
continuously
producing
adenosine
triphosphate,
they
also
stimulate
death
inducing
apoptosis
or
necroptosis
reperfused
myocardium.
Therefore,
defects
may
determine
fate
cardiomyocytes.
In
this
review,
we
summarize
regulatory
mechanisms
effects
myocardial
injury,
highlighting
potential
targets
for
clinical
management
reperfusion.
Biochemical and Biophysical Research Communications,
Journal Year:
2019,
Volume and Issue:
520(3), P. 606 - 611
Published: Oct. 14, 2019
Ferroptosis
is
a
distinct
iron-dependent
mechanism
of
regulated
cell
death
recognized
in
cancer
and
ischemia/reperfusion
(I/R)
injury
different
organs.
It
has
been
reported
that
molecules
such
as
liproxstatin-1
(Lip-1)
inhibit
ferroptosis
promote
survival
however,
the
mechanisms
underlying
this
action
are
not
clearly
understood.
We
investigated
role
Lip-1
reducing
ischemic
myocardium.
Using
an
I/R
model
isolated
perfused
mice
hearts
which
was
given
at
onset
reperfusion,
we
found
protects
heart
by
myocardial
infarct
sizes
maintaining
mitochondrial
structural
integrity
function.
Further
investigation
revealed
Lip-1-induced
cardioprotection
mediated
reduction
VDAC1
levels
oligomerization,
but
VDAC2/3.
treatment
also
decreased
reactive
oxygen
species
production
rescued
antioxidant
GPX4
caused
stress.
Meanwhile,
Ca2+
retention
capacity
needed
to
induce
permeability
transition
pore
opening
did
change
with
treatment.
Thus,
report
induces
cardioprotective
effects
against
restoring
levels.
Journal of Diabetes Research,
Journal Year:
2021,
Volume and Issue:
2021, P. 1 - 10
Published: June 28, 2021
Ferroptosis
is
a
novel
form
of
nonapoptotic
regulated
cell
death
(RCD).
It
features
iron-dependent
lipid
peroxide
accumulation
accompanied
by
inadequate
redox
enzymes,
especially
glutathione
peroxidase
4
(GPX4).
RAS-selective
lethal
3
(RSL3),
erastin,
and
ferroptosis
inducing
56
(FIN56)
induce
via
different
manners
targeting
GPX4
function.
Acyl-CoA
synthetase
long-chain
family
(ACSL4),
lysophosphatidylcholine
acyltransferase
(LPCAT3),
lipoxygenases
(LOXs)
participate
in
the
production
peroxides.
Heat
shock
protein
B
member
1
(HSPB1)
nuclear
receptor
coactivator
(NCOA4)
regulate
iron
homeostasis
preventing
caused
high
concentration
intracellular
iron.
ubiquitous
our
body
as
it
exists
both
physiologic
pathogenic
processes.
involved
glucose-stimulated
insulin
secretion
(GSIS)
impairment
arsenic-induced
pancreatic
damage
pathogenesis
diabetes.
Moreover,
iron-sulfur
(Fe-S)
cluster
influence
each
other,
causing
mitochondrial
accumulation,
more
reactive
oxygen
species
(ROS)
production,
endoplasmic
reticulum
(ER)
stress,
failure
biosynthesis
insulin,
β-cells.
In
addition,
also
engages
diabetic
complications
such
myocardial
ischemia
cardiomyopathy
(DCM).
this
review,
we
summarize
mechanism
its
association
with
type
2
diabetes
mellitus
(T2DM).
Signal Transduction and Targeted Therapy,
Journal Year:
2022,
Volume and Issue:
7(1)
Published: Feb. 23, 2022
Abstract
Ischemic
stroke
represents
a
significant
danger
to
human
beings,
especially
the
elderly.
Interventions
are
only
available
remove
clot,
and
mechanism
of
neuronal
death
during
ischemic
is
still
in
debate.
Ferroptosis
increasingly
appreciated
as
cell
after
ischemia
various
organs.
Here
we
report
that
serine
protease,
thrombin,
instigates
ferroptotic
signaling
by
promoting
arachidonic
acid
mobilization
subsequent
esterification
gene,
acyl-CoA
synthetase
long-chain
family
member
4
(ACSL4).
An
unbiased
multi-omics
approach
identified
thrombin
ACSL4
genes/proteins,
their
pro-ferroptotic
phosphatidylethanolamine
lipid
products,
prominently
altered
upon
middle
cerebral
artery
occlusion
rodents.
Genetically
or
pharmacologically
inhibiting
multiple
points
this
pathway
attenuated
outcomes
models
vitro
vivo.
Therefore,
thrombin-ACSL4
axis
may
be
key
therapeutic
target
ameliorate
injury
stroke.
