Cell Death and Disease,
Год журнала:
2019,
Номер
10(11)
Опубликована: Ноя. 4, 2019
Abstract
Ischaemic
heart
disease
(IHD)
is
the
leading
cause
of
death
worldwide.
Although
myocardial
cell
plays
a
significant
role
in
infarction
(MI),
its
underlying
mechanism
remains
to
be
elucidated.
To
understand
progression
MI
and
identify
potential
therapeutic
targets,
we
performed
tandem
mass
tag
(TMT)-based
quantitative
proteomic
analysis
using
an
mouse
model.
Gene
ontology
(GO)
gene
set
enrichment
(GSEA)
revealed
that
glutathione
metabolic
pathway
reactive
oxygen
species
(ROS)
were
significantly
downregulated
during
MI.
In
particular,
peroxidase
4
(GPX4),
which
protects
cells
from
ferroptosis
(an
iron-dependent
programme
regulated
necrosis),
was
early
middle
stages
RNA-seq
qRT-PCR
analyses
suggested
GPX4
downregulation
occurred
at
transcriptional
level.
Depletion
or
inhibition
specific
siRNA
chemical
inhibitor
RSL3,
respectively,
resulted
accumulation
lipid
peroxide,
by
H9c2
cardiomyoblasts.
neonatal
rat
ventricular
myocytes
(NRVMs)
less
sensitive
than
cells,
NRVMs
rapidly
underwent
response
under
cysteine
deprivation.
Our
study
suggests
contributes
ferroptotic
cardiomyocytes
upon
stress
such
as
Cell Death and Disease,
Год журнала:
2023,
Номер
14(10)
Опубликована: Окт. 4, 2023
Abstract
Autophagy
is
the
process
by
which
cells
degrade
and
recycle
proteins
organelles
to
maintain
intracellular
homeostasis.
Generally,
autophagy
plays
a
protective
role
in
cells,
but
disruption
of
mechanisms
or
excessive
autophagic
flux
usually
leads
cell
death.
Despite
recent
progress
study
regulation
underlying
molecular
autophagy,
numerous
questions
remain
be
answered.
How
does
regulate
death?
What
are
fine-tuned
regulatory
autophagy-dependent
death
(ADCD)
autophagy-mediated
(AMCD)?
In
this
article,
we
highlight
different
roles
discuss
six
main
autophagy-related
modalities,
with
focus
on
metabolic
changes
caused
endoplasmic
reticulum-phagy
(ER-phagy)-induced
mitophagy
ferroptosis.
Finally,
enhancement
treatment
diseases
offer
new
perspective
based
use
for
functional
conversions
(including
conversion
that
modalities)
clinical
tumors.
Oxidative Medicine and Cellular Longevity,
Год журнала:
2021,
Номер
2021(1)
Опубликована: Янв. 1, 2021
Reactive
oxygen
species
(ROS)
are
essential
for
cellular
signaling
and
response
to
stress.
The
level
of
ROS
the
type
determine
ability
cells
undergo
cell
death.
Furthermore,
dysregulation
antioxidant
pathways
is
associated
with
many
diseases.
It
has
become
apparent
that
death
can
occur
through
different
mechanisms
leading
classifications
types
such
as
apoptosis,
ferroptosis,
necroptosis.
play
roles
in
all
forms
death,
but
it
only
now
coming
into
focus
control
occurs
any
given
cell.
Indeed,
may
act
a
rheostat
allowing
be
engaged
crosstalk
types.
In
this
review,
we
will
describe
regulatory
how
they
under
normal
disease
states.
We
also
propose
could
provide
mechanism
between
determining
Cell Death and Disease,
Год журнала:
2019,
Номер
10(11)
Опубликована: Ноя. 4, 2019
Abstract
Ischaemic
heart
disease
(IHD)
is
the
leading
cause
of
death
worldwide.
Although
myocardial
cell
plays
a
significant
role
in
infarction
(MI),
its
underlying
mechanism
remains
to
be
elucidated.
To
understand
progression
MI
and
identify
potential
therapeutic
targets,
we
performed
tandem
mass
tag
(TMT)-based
quantitative
proteomic
analysis
using
an
mouse
model.
Gene
ontology
(GO)
gene
set
enrichment
(GSEA)
revealed
that
glutathione
metabolic
pathway
reactive
oxygen
species
(ROS)
were
significantly
downregulated
during
MI.
In
particular,
peroxidase
4
(GPX4),
which
protects
cells
from
ferroptosis
(an
iron-dependent
programme
regulated
necrosis),
was
early
middle
stages
RNA-seq
qRT-PCR
analyses
suggested
GPX4
downregulation
occurred
at
transcriptional
level.
Depletion
or
inhibition
specific
siRNA
chemical
inhibitor
RSL3,
respectively,
resulted
accumulation
lipid
peroxide,
by
H9c2
cardiomyoblasts.
neonatal
rat
ventricular
myocytes
(NRVMs)
less
sensitive
than
cells,
NRVMs
rapidly
underwent
response
under
cysteine
deprivation.
Our
study
suggests
contributes
ferroptotic
cardiomyocytes
upon
stress
such
as