Medicinal Research Reviews,
Journal Year:
2021,
Volume and Issue:
42(1), P. 259 - 305
Published: May 6, 2021
Abstract
Ischemic
stroke
caused
by
arterial
occlusion
is
the
most
common
type
of
stroke,
which
among
frequent
causes
disability
and
death
worldwide.
Current
treatment
approaches
involve
achieving
rapid
reperfusion
either
pharmacologically
or
surgically,
both
are
time‐sensitive;
moreover,
blood
flow
recanalization
often
ischemia/reperfusion
injury.
However,
even
though
neuroprotective
intervention
urgently
needed
in
event
exact
mechanisms
neuronal
during
ischemic
still
unclear,
consequently,
capacity
for
drug
development
has
remained
limited.
Multiple
cell
pathways
implicated
pathogenesis
stroke.
Here,
we
have
reviewed
these
potential
pathways,
including
intrinsic
extrinsic
apoptosis,
necroptosis,
autophagy,
ferroptosis,
parthanatos,
phagoptosis,
pyroptosis.
We
also
latest
results
pharmacological
studies
on
summarized
emerging
targets
with
a
focus
clinical
trials.
These
observations
may
help
to
further
understand
pathological
events
bridge
gap
between
basic
translational
research
reveal
novel
interventions.
Cell Death and Disease,
Journal Year:
2023,
Volume and Issue:
14(3)
Published: March 21, 2023
Abstract
Ferroptosis
is
an
iron-dependent
regulated
cell
death
driven
by
excessive
lipid
peroxidation.
Inflammation
one
common
and
effective
physiological
event
that
protects
against
various
stimuli
to
maintain
tissue
homeostasis.
However,
the
dysregulation
of
inflammatory
responses
can
cause
imbalance
immune
system,
dysfunction
death.
Recent
studies
have
pointed
out
activation
inflammation,
including
multiple
inflammation-related
signaling
pathways,
lead
ferroptosis.
Among
related
signal
transduction
we
focused
on
five
classical
namely,
JAK-STAT,
NF-κB,
inflammasome,
cGAS-STING
MAPK
expounded
their
roles
in
To
date,
many
agents
shown
therapeutic
effects
ferroptosis-related
diseases
modulating
aforementioned
pathways
vivo
vitro.
Moreover,
regulatory
these
iron
metabolism
peroxidation
been
described
detail,
contributing
further
understanding
pathophysiological
process
Taken
together,
targeting
inflammation
will
provide
appropriate
ways
intervene
ferroptosis
diseases.
Cells,
Journal Year:
2021,
Volume and Issue:
10(3), P. 515 - 515
Published: Feb. 28, 2021
Heme
oxygenase
catalyzes
the
rate-limiting
step
in
heme
degradation
order
to
generate
biliverdin,
carbon
monoxide
(CO),
and
iron.
The
inducible
form
of
enzyme,
oxygenase-1
(HO-1),
exerts
a
central
role
cellular
protection.
substrate,
heme,
is
potent
pro-oxidant
that
can
accelerate
inflammatory
injury
promote
cell
death.
HO-1
has
been
implicated
as
key
mediator
tissue
injury,
validated
preclinical
models
acute
lung
sepsis.
A
large
body
work
also
cytoprotective
molecule
against
various
forms
death,
including
necrosis,
apoptosis
newly
recognized
regulated
death
(RCD)
programs
such
necroptosis,
pyroptosis,
ferroptosis.
While
antiapoptotic
potential
its
reaction
product
CO
regulation
extensively
characterized,
relatively
fewer
studies
have
explored
regulatory
other
necrotic
RCD
(i.e.,
necroptosis
ferroptosis).
may
provide
anti-inflammatory
protection
or
pyroptosis.
In
contrast,
ferroptosis,
play
pro-death
via
enhancing
iron
release.
co-regulation
autophagy,
homeostatic
program
for
catabolic
recycling
proteins
organelles.
autophagy
primarily
associated
with
survival,
occurrence
coincide
programs.
This
review
will
summarize
roles
products
co-regulating
programs,
implication
both
protective
detrimental
responses,
emphasis
on
how
these
impact
candidate
therapeutic
target
disease.
Experimental & Molecular Medicine,
Journal Year:
2023,
Volume and Issue:
55(8), P. 1595 - 1619
Published: Aug. 23, 2023
Abstract
Mitochondria,
ubiquitous
double-membrane-bound
organelles,
regulate
energy
production,
support
cellular
activities,
harbor
metabolic
pathways,
and,
paradoxically,
mediate
cell
fate.
Evidence
has
shown
mitochondria
as
points
of
convergence
for
diverse
death-inducing
pathways
that
trigger
the
various
mechanisms
underlying
apoptotic
and
nonapoptotic
programmed
death.
Thus,
dysfunctional
eventually
lead
or
contribute
to
age-related
diseases,
such
neurodegenerative,
cardiovascular
diseases.
mitochondrion-associated
death-based
treatments
show
great
therapeutic
potential,
providing
novel
insights
in
clinical
trials.
This
review
discusses
mitochondrial
quality
control
networks
with
activity
triggered
by
stimuli
maintain
homeostasis
via
mitohormesis,
unfolded
protein
response,
mitophagy.
The
also
presents
details
on
forms
mitochondria-associated
death,
including
apoptosis,
necroptosis,
ferroptosis,
pyroptosis,
parthanatos,
paraptosis,
highlights
their
involvement
disease
pathogenesis,
collectively
suggesting
directions
further
research.
