Biomedicine & Pharmacotherapy,
Journal Year:
2022,
Volume and Issue:
153, P. 113374 - 113374
Published: July 11, 2022
Non-alcoholic
fatty
liver
disease
(NAFLD)
is
a
public
health
problem
associated
with
high
mortality
and
morbidity
rates
worldwide.
Presently,
its
complex
pathophysiology
still
unclear,
there
no
specific
drug
to
reverse
NAFLD.
Ferroptosis
an
iron-dependent
non-apoptotic
form
of
cell
death
characterized
by
the
iron-induced
accumulation
lipid
reactive
oxygen
species
(ROS),
which
damage
nucleic
acids,
proteins,
lipids;
generate
intracellular
oxidative
stress;
ultimately
cause
death.
Emerging
evidence
indicates
that
ferroptosis
involved
in
progression
NAFLD,
although
mechanism
action
NAFLD
poorly
understood.
Herein,
we
summarize
certain
diseases,
especially
pathogenesis
discuss
potential
therapeutic
approaches
currently
used
treat
This
review
also
highlights
further
directions
for
treatment
prevention
related
diseases.
Biomedicine & Pharmacotherapy,
Journal Year:
2020,
Volume and Issue:
127, P. 110108 - 110108
Published: March 29, 2020
Ferroptosis
is
a
newly
discovered
type
of
cell
death
triggered
by
intracellular
phospholipid
peroxidation
that
morphologically,
biologically
and
genetically
distinct
from
other
types
death.
classified
as
regulated
necrosis
more
immunogenic
than
apoptosis.
To
date,
compelling
evidence
indicates
ferroptosis
plays
an
important
role
in
inflammation,
several
antioxidants
functioning
inhibitors
have
been
shown
to
exert
anti-inflammatory
effects
experimental
models
certain
diseases.
Our
review
provides
overview
the
link
between
inflammation;
better
understanding
mechanisms
underlying
inflammation
may
hasten
development
promising
therapeutic
strategies
involving
address
inflammation.
Cells,
Journal Year:
2020,
Volume and Issue:
9(6), P. 1505 - 1505
Published: June 20, 2020
Ferroptosis
is
a
new
type
of
oxidative
regulated
cell
death
(RCD)
driven
by
iron-dependent
lipid
peroxidation.
As
major
sites
iron
utilization
and
master
regulators
metabolism,
mitochondria
are
the
main
source
reactive
oxygen
species
(ROS)
and,
thus,
play
role
in
this
RCD.
is,
indeed,
associated
with
severe
damage
mitochondrial
morphology,
bioenergetics,
metabolism.
Furthermore,
dysregulation
metabolism
considered
biochemical
feature
neurodegenerative
diseases
linked
to
ferroptosis.
Whether
dysfunction
can,
per
se,
initiate
ferroptosis
whether
function
context-dependent
still
under
debate.
Cancer
cells
accumulate
high
levels
ROS
promote
their
metabolic
activity
growth.
Of
note,
cancer
rewiring
often
acquired
sensitivity
This
strongly
suggests
that
may
act
as
an
adaptive
response
imbalance
constitute
promising
way
eradicate
malignant
cells.
Here,
we
review
current
literature
on
ferroptosis,
discuss
opportunities
potentially
use
mitochondria-mediated
strategy
for
therapy.
Cell Death and Disease,
Journal Year:
2021,
Volume and Issue:
12(4)
Published: March 17, 2021
Ferroptosis
is
a
newly
recognised
type
of
regulated
cell
death
(RCD)
characterised
by
iron-dependent
accumulation
lipid
peroxidation.
It
significantly
distinct
from
other
RCDs
at
the
morphological,
biochemical,
and
genetic
levels.
Recent
reports
have
implicated
ferroptosis
in
multiple
diseases,
including
neurological
disorders,
kidney
injury,
liver
cancer.
Ferroptotic
has
also
been
associated
with
dysfunction
intestinal
epithelium,
which
contributes
to
several
diseases.
Research
on
may
provide
new
understanding
disease
pathogenesis
that
benefits
clinical
treatment.
In
this
review,
we
an
overview
its
underlying
mechanisms,
then
describe
emerging
role
ischaemia/reperfusion
(I/R)
inflammatory
bowel
(IBD),
colorectal
cancer
(CRC).
Biomolecules,
Journal Year:
2021,
Volume and Issue:
11(4), P. 589 - 589
Published: April 16, 2021
Heme-oxygenase
is
the
enzyme
responsible
for
degradation
of
endogenous
iron
protoporphyirin
heme;
it
catalyzes
reaction's
rate-limiting
step,
resulting
in
release
carbon
monoxide
(CO),
ferrous
ions,
and
biliverdin
(BV),
which
successively
reduced
bilirubin
(BR)
by
reductase.
Several
studies
have
drawn
attention
to
controversial
role
HO-1,
inducible
isoform,
pointing
out
its
implications
cancer
other
diseases
development,
but
also
underlining
importance
antioxidant
activity.
The
contribution
HO-1
redox
homeostasis
leads
a
relevant
decrease
cells
oxidative
damage,
can
be
reconducted
cytoprotective
effects
explicated
alongside
mechanisms
involving
genes
like
TIGAR
(TP53-induced
glycolysis
apoptosis
regulator),
therapeutic
functions
heme
main
transformation
products,
especially
has
been
shown
effective
on
GSH
levels
implementation
sustaining
body's
response
stress.
aim
this
review
was
collect
most
knowledge
from
literature,
analyzing
different
perspectives
try
put
forward
hypothesis
revealing
yet
unknown
HO-1-involved
pathways
that
could
useful
promote
development
new
therapeutical
strategies,
lay
foundation
further
investigation
fully
understand
important
system.
Molecular Cancer,
Journal Year:
2022,
Volume and Issue:
21(1)
Published: Jan. 28, 2022
Abstract
N6-methyladenosine
(m6A)
methylation,
the
most
common
form
of
internal
RNA
modification
in
eukaryotes,
has
gained
increasing
attention
and
become
a
hot
research
topic
recent
years.
M6A
plays
multifunctional
roles
normal
abnormal
biological
processes,
its
role
may
vary
greatly
depending
on
position
m6A
motif.
Programmed
cell
death
(PCD)
includes
apoptosis,
autophagy,
pyroptosis,
necroptosis
ferroptosis,
which
involve
breakdown
plasma
membrane.
Based
implications
methylation
PCD,
regulators
functional
were
comprehensively
studied
reported.
In
this
review,
we
focus
high-complexity
links
between
different
types
PCD
pathways,
are
then
closely
associated
with
initiation,
progression
resistance
cancer.
Herein,
clarifying
relationship
is
great
significance
to
provide
novel
strategies
for
cancer
treatment,
potential
prospect
clinical
application.
