Antioxidants and Redox Signaling,
Journal Year:
2023,
Volume and Issue:
39(10-12), P. 708 - 727
Published: July 14, 2023
Significance:
Redox
signaling
through
mitochondrial
reactive
oxygen
species
(mtROS)
has
a
key
role
in
several
mechanisms
of
regulated
cell
death
(RCD),
necroptosis,
ferroptosis,
pyroptosis,
and
apoptosis,
thereby
decisively
contributing
to
inflammatory
disorders.
The
mtROS
apoptosis
been
extensively
addressed,
but
their
involvement
necrotic-like
RCD
just
started
being
elucidated,
providing
novel
insights
into
the
pathophysiology
acute
inflammation.
Recent
Advances:
p53
together
with
drive
necroptosis
inflammation
downregulation
sulfiredoxin
peroxiredoxin
3.
Mitochondrial
hydroorotate
dehydrogenase
is
redox
system
regulation
ferroptosis.
In
addition,
noncanonical
pathway,
which
generates
Ragulator-Rag
complex
acts
via
mTORC1
promote
gasdermin
D
oligomerization,
triggers
pyroptosis.
Critical
Issues:
trigger
positive
feedback
loops
leading
lytic
conjunction
necrosome,
inflammasome,
glutathione
depletion,
peroxidase
4
deficiency.
Future
Directions:
precise
mechanism
membrane
rupture
ferroptosis
contribution
disorders
are
still
unclear,
will
need
further
research.
antioxidants
may
provide
promising
therapeutic
approaches
toward
However,
establishing
doses
windows
action
be
required
optimize
potential,
avoid
potential
adverse
side
effects
linked
blockade
beneficial
adaptive
signaling.
Antioxid.
Signal.
39,
708-727.
Journal of Inflammation Research,
Journal Year:
2023,
Volume and Issue:
Volume 16, P. 4073 - 4085
Published: Sept. 1, 2023
Abstract:
Ferroptosis,
a
programmed
cell
death
discovered
in
recent
years,
is
an
iron-dependent
lipid
peroxidation
accumulation.
Unlike
other
modes
of
(autophagy,
necroptosis,
pyroptosis,
cuproptosis,
etc.),
ferroptosis
has
unique
morphological
characteristics
and
plays
important
role
variety
diseases.
In
there
been
great
progress
the
study
ferroptosis.
Studies
have
found
that
associated
with
acute
lung
injury
(ALI),
condition
high
mortality
rate
limited
treatment
options.
This
paper
summarizes
mechanism
from
perspectives
iron
metabolism,
amino
acid
glutathione
metabolism.
It
also
discusses
research
ALI
order
to
find
new
directions
for
prevention
this
condition.
Keywords:
ferroptosis,
injury,
ischemia,
sepsis,
targeted
therapy
Shock,
Journal Year:
2022,
Volume and Issue:
57(6), P. 274 - 281
Published: May 17, 2022
ABSTRACT
The
effects
of
ferroptosis,
an
iron-dependent
cell
death,
on
acute
respiratory
distress
syndrome
(ARDS)
remain
largely
elusive.
Hepcidin,
encoded
by
the
HAMP
gene,
affects
inflammation,
and
iron
homeostasis.
present
study
aimed
to
investigate
whether
hepcidin
protects
against
ferroptosis
in
lipopolysaccharide
(LPS)-induced
ARDS.
Our
results
confirmed
that
aggravated
lung
inflammation
damage
LPS-induced
Hepcidin
defended
with
similar
those
inhibitor
ferrostatin-1
(Fer-1).
Moreover,
decreased
uptake,
as
determined
Transferrin
Receptor
1
(TfR1)
expression
levels,
increased
storage,
based
ferritin
heavy
chain
(FTH)
expression.
A549
line
were
vivo
results.
In
addition,
we
used
si-FTH
knock
down
FTH
found
this
suppressed
ability
protect
ferroptosis.
Collectively,
our
data
suggest
inhibits
increasing
ARDS;
thus,
may
represent
a
possible
treatment
targeting
Antioxidants and Redox Signaling,
Journal Year:
2023,
Volume and Issue:
39(10-12), P. 708 - 727
Published: July 14, 2023
Significance:
Redox
signaling
through
mitochondrial
reactive
oxygen
species
(mtROS)
has
a
key
role
in
several
mechanisms
of
regulated
cell
death
(RCD),
necroptosis,
ferroptosis,
pyroptosis,
and
apoptosis,
thereby
decisively
contributing
to
inflammatory
disorders.
The
mtROS
apoptosis
been
extensively
addressed,
but
their
involvement
necrotic-like
RCD
just
started
being
elucidated,
providing
novel
insights
into
the
pathophysiology
acute
inflammation.
Recent
Advances:
p53
together
with
drive
necroptosis
inflammation
downregulation
sulfiredoxin
peroxiredoxin
3.
Mitochondrial
hydroorotate
dehydrogenase
is
redox
system
regulation
ferroptosis.
In
addition,
noncanonical
pathway,
which
generates
Ragulator-Rag
complex
acts
via
mTORC1
promote
gasdermin
D
oligomerization,
triggers
pyroptosis.
Critical
Issues:
trigger
positive
feedback
loops
leading
lytic
conjunction
necrosome,
inflammasome,
glutathione
depletion,
peroxidase
4
deficiency.
Future
Directions:
precise
mechanism
membrane
rupture
ferroptosis
contribution
disorders
are
still
unclear,
will
need
further
research.
antioxidants
may
provide
promising
therapeutic
approaches
toward
However,
establishing
doses
windows
action
be
required
optimize
potential,
avoid
potential
adverse
side
effects
linked
blockade
beneficial
adaptive
signaling.
Antioxid.
Signal.
39,
708-727.
