Journal of Bioenergetics and Biomembranes,
Год журнала:
2024,
Номер
56(4), С. 405 - 418
Опубликована: Июнь 6, 2024
Abstract
Background
Ferritinophagy-mediated
ferroptosis
plays
a
crucial
role
in
fighting
pathogen
aggression.
The
long
non-coding
RNA
Mir22hg
is
involved
the
regulation
of
and
aberrantly
overexpression
lipopolysaccharide
(LPS)-induced
sepsis
mice,
but
whether
it
regulates
through
ferritinophagy-mediated
unclear.
Methods
was
screened
by
bioinformatics
analysis.
Ferroptosis
assessed
assaying
malondialdehyde
(MDA),
reactive
oxygen
species
(ROS),
Fe
2+
levels,
glutathione
(GSH)
activity,
as
well
ferroptosis-related
proteins
GPX4
SLC3A2
using
matched
kits
performing
western
blot.
Ferritinophagy
Lyso
tracker
staining
FerroOrange
staining,
immunofluorescence
analysis
Ferritin
LC-3,
blot
LC-3II/I,
p62,
FTH1,
NCOA4.
bind
YTH
domain
containing
1
(YTHDC1)
to
or
angiopoietin-like-4
(Angptl4)
verified
pull-down
and/or
immunoprecipitation
(RIP)
assays.
Results
silencing
lightened
ferritinophagy
LPS-induced
MLE-12
cells
mouse
models,
presented
downregulated
MDA,
ROS,
,
NCOA4,
upregulated
GPX4,
GSH,
FTH1
along
with
decrease
autophagy.
could
m6A
reader
YTHDC1
without
affecting
its
expression.
Mechanistically,
enhanced
Angptl4
mRNA
stability
recruiting
YTHDC1.
Furthermore,
partly
overturned
inhibition-mediated
effects
on
cells.
Conclusion
contributed
via
strengthening
stability,
highlighting
that
may
be
potential
target
for
treatment
based
ferroptosis.
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.
International Journal of Biological Sciences,
Год журнала:
2024,
Номер
20(9), С. 3621 - 3637
Опубликована: Янв. 1, 2024
Ferroptosis,
an
emerging
type
of
programmed
cell
death,
is
initiated
by
iron-dependent
and
excessive
ROS-mediated
lipid
peroxidation,
which
eventually
leads
to
plasma
membrane
rupture
death.
Many
canonical
signalling
pathways
biological
processes
are
involved
in
ferroptosis.
Furthermore,
cancer
cells
more
susceptible
ferroptosis
due
the
high
load
ROS
unique
metabolic
characteristics,
including
iron
requirements.
Recent
investigations
have
revealed
that
plays
a
crucial
role
progression
tumours,
especially
HCC.
Specifically,
induction
can
not
only
inhibit
growth
hepatoma
cells,
thereby
reversing
tumorigenesis,
but
also
improves
efficacy
immunotherapy
enhances
antitumour
immune
response.
Therefore,
triggering
has
become
new
therapeutic
strategy
for
therapy.
In
this
review,
we
summarize
characteristics
based
on
its
underlying
mechanism
HCC
provide
possible
applications.
Frontiers in Pharmacology,
Год журнала:
2024,
Номер
15
Опубликована: Апрель 26, 2024
Liver
cancer
is
the
second
leading
cause
of
cancer-related
death
worldwide.
However,
treatment
options,
including
surgical
resection,
transplantation,
and
molecular
drug
therapies,
are
limited
effectiveness.
Recent
studies
have
demonstrated
that
suppressing
ferroptosis
might
be
a
pivotal
signal
for
liver
initiation,
thus
providing
new
way
to
combat
cancer.
Ferroptosis
distinct
form
controlled
cell
differs
from
conventional
routes
like
apoptosis,
necrosis,
pyroptosis.
It
results
intracellular
iron
overload,
which
raises
iron-dependent
reactive
oxygen
species.
This,
in
turn,
leads
accumulation
lipid
peroxides
further
result
oxidative
damage
membranes,
disrupt
normal
functioning,
ultimately
speed
up
phenomenon.
regulation
intricately
linked
cellular
physiological
processes,
encompassing
metabolism,
equilibrium
between
oxygen-free
radical
reactions
peroxidation.
This
review
intends
summarize
natural
compounds
targeting
offer
therapeutic
ideas
Furthermore,
it
serves
as
foundation
identifying
applying
chemical
medicines
chemicals
target
treat
efficiently.
International Journal of Biological Sciences,
Год журнала:
2025,
Номер
21(4), С. 1837 - 1851
Опубликована: Фев. 10, 2025
Radiotherapy
is
the
primary
treatment
for
nasopharyngeal
carcinoma
(NPC);
nonetheless,
radioresistance
remains
leading
cause
of
localized
recurrence.
Our
study
demonstrates
a
significant
increase
in
N6-methyladenosine
(m6A)
methylase
METTL3
NPC
and
other
tumors.
Mechanistically,
acts
as
an
m6A
methylase,
enhancing
modification
solute
carrier
family
7
member
11
(SLC7A11)
transcript,
which
increases
its
stability
expression,
thereby
inhibiting
radiation-induced
ferroptosis
ultimately
inducing
NPC.
Furthermore,
silencing
SLC7A11
or
employing
inducer
Erastin
negated
promoting
effect
on
cell
radioresistance.
These
findings
suggest
that
could
be
novel
therapeutic
target
overcoming
radiotherapy
resistance
The FASEB Journal,
Год журнала:
2022,
Номер
36(12)
Опубликована: Ноя. 18, 2022
To
explore
the
effect
of
curcumol
on
autophagy
and
ferroptosis
hepatic
stellate
cells,
to
clarify
molecular
mechanism
its
anti-hepatic
fibrosis.
In
present
study,
we
report
that
promotes
death
activated
HSCs
reduces
deposition
extracellular
matrix.
Interestingly,
treatment
can
trigger
eliminate
characterized
by
iron
overload,
lipid
ROS
accumulation,
glutathione
depletion,
peroxidation.
Curcumol
HSC
autophagy,
which
may
be
key
for
induction
ferroptosis.
It
is
worth
noting
upregulation
nuclear
receptor
coactivator
4
(NCOA4)
play
a
mechanism.
NCOA4
mediates
release
ions
induces
occurrence
Overall,
in
degradation
FTH1
complexes,
releases
ions,
leads
ferroptosis,
an
important
fibrosis
effect.