Ecotoxicology and Environmental Safety,
Год журнала:
2024,
Номер
280, С. 116553 - 116553
Опубликована: Июнь 7, 2024
The
incidence
of
nonalcoholic
steatohepatitis
(NASH)
is
related
with
perfluorooctane
sulfonate
(PFOS),
yet
the
mechanism
remains
ill-defined.
Mounting
evidence
suggests
that
ferroptosis
plays
a
crucial
role
in
initiation
NASH.
In
this
study,
we
used
mice
and
human
hepatocytes
L-02
to
investigate
PFOS-induced
NASH
effect
molecular
PFOS
on
liver
ferroptosis.
We
found
here
caused
mice,
lipid
accumulation
inflammatory
response
cells.
induced
hepatic
vivo
vitro,
as
evidenced
by
decrease
glutathione
peroxidase
4
(GPX4),
increases
cytosolic
iron,
acyl-CoA
synthetase
long-chain
family
member
(ACSL4)
peroxidation.
PFOS-treated
cells,
factors
contents
were
reversed
inhibitor.
was
relieved
autophagy
expression
mitochondrial
calcium
uniporter
(MCU)
accelerated
PFOS,
leading
subsequent
accumulation,
inhibiting
increase
MCU.
Inhibiting
variations
GPX4
without
influencing
change
ACSL4,
PFOS.
MCU
interacted
ACSL4
siRNA
against
changes
ACSL4，GPX4
iron
systemically.
This
study
put
forward
involvement
identified
mediator
autophagy-dependent
Chinese Medical Journal,
Год журнала:
2023,
Номер
unknown
Опубликована: Июль 6, 2023
Long-chain
acyl-coenzyme
A
(CoA)
synthase
4
(ACSL4)
is
an
enzyme
that
esterifies
CoA
into
specific
polyunsaturated
fatty
acids,
such
as
arachidonic
acid
and
adrenic
acid.
Based
on
accumulated
evidence,
the
ACSL4-catalyzed
biosynthesis
of
arachidonoyl-CoA
contributes
to
execution
ferroptosis
by
triggering
phospholipid
peroxidation.
Ferroptosis
a
type
programmed
cell
death
caused
iron-dependent
peroxidation
lipids;
ACSL4
glutathione
peroxidase
positively
negatively
regulate
ferroptosis,
respectively.
In
addition,
essential
regulator
(FA)
metabolism.
remodels
composition
membranes,
regulates
steroidogenesis,
balances
eicosanoid
biosynthesis.
ACSL4-mediated
metabolic
reprogramming
antitumor
immunity
have
attracted
much
attention
in
cancer
biology.
Because
it
facilitates
cross-talk
between
FA
metabolism,
also
research
hotspot
diseases
ischemia/reperfusion
injuries.
this
review,
we
focus
structure,
biological
function,
unique
role
ASCL4
various
human
diseases.
Finally,
propose
might
be
potential
therapeutic
target.
Autophagy,
Год журнала:
2024,
Номер
20(6), С. 1213 - 1246
Опубликована: Март 6, 2024
Macroautophagy/autophagy
is
a
complex
degradation
process
with
dual
role
in
cell
death
that
influenced
by
the
types
are
involved
and
stressors
they
exposed
to.
Ferroptosis
an
iron-dependent
oxidative
form
of
characterized
unrestricted
lipid
peroxidation
context
heterogeneous
plastic
mechanisms.
Recent
studies
have
shed
light
on
involvement
specific
autophagy
(e.g.
ferritinophagy,
lipophagy,
clockophagy)
initiating
or
executing
ferroptotic
through
selective
anti-injury
proteins
organelles.
Conversely,
other
forms
reticulophagy
lysophagy)
enhance
cellular
defense
against
damage.
Dysregulated
autophagy-dependent
ferroptosis
has
implications
for
diverse
range
pathological
conditions.
This
review
aims
to
present
updated
definition
ferroptosis,
discuss
influential
substrates
receptors,
outline
experimental
methods,
propose
guidelines
interpreting
results.
Drug
resistance
is
a
common
challenge
in
clinical
tumor
treatment.
A
reduction
drug
sensitivity
of
cells
often
accompanied
by
an
increase
autophagy
levels,
leading
to
autophagy-related
resistance.
The
effectiveness
combining
chemotherapy
drugs
with
inducers/inhibitors
has
been
widely
confirmed,
but
the
mechanisms
are
still
unclear.
Ferroptosis
and
pyroptosis
can
be
affected
various
types
autophagy.
Therefore,
ferroptosis
have
crosstalk
via
autophagy,
potentially
switch
cell
death
under
certain
conditions.
As
two
forms
inflammatory
programmed
death,
different
effects
on
inflammation,
cGAS-STING
signaling
pathway
also
involved.
it
plays
important
role
progression
some
chronic
diseases.
This
review
discusses
relationship
between
pyroptosis,
attempts
uncover
reasons
behind
evasion
nature
Chaperone-mediated
autophagy
(CMA)
is
a
lysosomal
degradation
pathway
that
eliminates
substrate
proteins
through
heat-shock
cognate
protein
70
recognition
and
lysosome-associated
membrane
type
2A-assisted
translocation.
It
distinct
from
macroautophagy
microautophagy.
In
recent
years,
the
regulatory
mechanisms
of
CMA
have
been
gradually
enriched,
including
newly
discovered
NRF2
p38-TFEB
signaling,
as
positive
negative
pathways
CMA,
respectively.
Normal
activity
involved
in
regulation
metabolism,
aging,
immunity,
cell
cycle,
other
physiological
processes,
while
dysfunction
may
be
occurrence
neurodegenerative
disorders,
tumors,
intestinal
atherosclerosis,
so
on,
which
provides
potential
targets
for
treatment
prediction
related
diseases.
This
article
describes
general
process
its
role
activities
summarizes
connection
between
macroautophagy.
addition,
human
diseases
concern
or
protective
are
discussed.
Our
review
deepens
understanding
functions
summary
past
research
vision
future
directions.
Advanced Healthcare Materials,
Год журнала:
2023,
Номер
12(23)
Опубликована: Апрель 6, 2023
Increased
tissue
stiffness
is
associated
with
various
pathological
processes,
such
as
fibrosis,
inflammation,
and
aging.
The
matrix
of
the
nucleus
pulposus
(NP)
tissues
increases
gradually
during
intervertebral
disc
degeneration
(IDD),
while
mechanism
through
which
NP
cells
sense
react
to
remains
unclear.
In
this
study,
results
indicate
that
ferroptosis
involved
in
stiff
substrate-induced
cell
death.
expression
acyl-CoA
synthetase
long-chain
family
member
4
(ACSL4)
group,
mediates
lipid
peroxidation
cells.
addition,
substrate
activates
hippo
signaling
cascade
induces
nuclear
translocation
yes-associated
protein
(YAP).
Interestingly,
inhibition
YAP
efficient
reverse
increase
ACSL4
caused
by
stiffness.
Furthermore,
suppresses
N-cadherin
overexpression
can
inhibit
via
formation
N-cadherin/β-catenin/YAP
complex,
stiffness-induced
Finally,
effects
on
IDD
progression
are
further
illustrated
animal
models.
These
findings
reveal
a
new
mechanotransduction
cells,
providing
novel
insights
into
development
therapies
for
treatment
IDD.
Biology,
Год журнала:
2023,
Номер
12(6), С. 864 - 864
Опубликована: Июнь 15, 2023
Lipid
metabolism,
cell
death,
and
autophagy
are
interconnected
processes
in
cells.
Dysregulation
of
lipid
metabolism
can
lead
to
such
as
via
ferroptosis
apoptosis,
while
lipids
also
play
a
crucial
role
the
regulation
autophagosome
formation.
An
increased
autophagic
response
not
only
promotes
survival
but
causes
death
depending
on
context,
especially
when
selectively
degrading
antioxidant
proteins
or
organelles
that
promote
ferroptosis.
ACSL4
is
an
enzyme
catalyzes
formation
long-chain
acyl-CoA
molecules,
which
important
intermediates
biosynthesis
various
types
lipids.
found
many
tissues
particularly
abundant
brain,
liver,
adipose
tissue.
linked
variety
diseases,
including
cancer,
neurodegenerative
disorders,
cardiovascular
disease,
acute
kidney
injury,
metabolic
disorders
(such
obesity
non-alcoholic
fatty
liver
disease).
In
this
review,
we
introduce
structure,
function,
ACSL4;
discuss
its
ferroptosis,
autophagy;
summarize
pathological
function;
explore
potential
implications
targeting
treatment
diseases.
