Autophagy,
Journal Year:
2023,
Volume and Issue:
19(7), P. 1982 - 1996
Published: Jan. 9, 2023
Ferroptosis
is
a
type
of
iron-dependent
regulated
cell
death
characterized
by
unrestricted
lipid
peroxidation
and
membrane
damage.
Although
GPX4
(glutathione
peroxidase
4)
plays
master
role
in
blocking
ferroptosis
eliminating
phospholipid
hydroperoxides,
the
regulation
remains
poorly
understood.
Here,
we
report
an
unexpected
for
copper
promoting
ferroptotic
death,
but
not
cuproptosis,
inducing
macroautophagic/autophagic
degradation
GPX4.
Copper
chelators
reduce
sensitivity
do
inhibit
other
types
such
as
apoptosis,
necroptosis,
alkaliptosis.
Conversely,
exogenous
increases
ubiquitination
formation
aggregates
directly
binding
to
protein
cysteines
C107
C148.
TAX1BP1
(Tax1
1)
then
acts
autophagic
receptor
subsequent
response
stress.
Consequently,
enhances
ferroptosis-mediated
tumor
suppression
mouse
model
pancreatic
cancer
tumor,
whereas
attenuate
experimental
acute
pancreatitis
associated
with
ferroptosis.
Taken
together,
these
findings
provide
new
insights
into
link
between
metal
stress
autophagy-dependent
death.Abbreviations:
CALCOCO2,
calcium
coiled-coil
domain
2;
GPX4,
glutathione
4;
MAP1LC3A/B,
microtubule
1
light
chain
3
alpha/beta;
MPO,
myeloperoxidase;
NCOA4,
nuclear
coactivator
OPTN,
optineurin;
PDAC,
ductal
adenocarcinoma;
RIPK1,
interacting
serine/threonine
kinase
1;
ROS,
reactive
oxygen
species;
SLC40A1,
solute
carrier
family
40
member
SQSTM1,
sequestosome
TAX1BP1,
Tax1
TEPA,
tetraethylenepentamine;
TM,
tetrathiomolybdate.
Autophagy,
Journal Year:
2023,
Volume and Issue:
19(8), P. 2175 - 2195
Published: April 14, 2023
Copper
is
an
essential
trace
element
in
biological
systems,
maintaining
the
activity
of
enzymes
and
function
transcription
factors.
However,
at
high
concentrations,
copper
ions
show
increased
toxicity
by
inducing
regulated
cell
death,
such
as
apoptosis,
paraptosis,
pyroptosis,
ferroptosis,
cuproptosis.
Furthermore,
can
trigger
macroautophagy/autophagy,
a
lysosome-dependent
degradation
pathway
that
plays
dual
role
regulating
survival
or
death
fate
cells
under
various
stress
conditions.
Pathologically,
impaired
metabolism
due
to
environmental
genetic
causes
implicated
variety
human
diseases,
rare
Wilson
disease
common
cancers.
Therapeutically,
copper-based
compounds
are
potential
chemotherapeutic
agents
be
used
alone
combination
with
other
drugs
approaches
treat
cancer.
Here,
we
review
progress
made
understanding
metabolic
processes
their
impact
on
regulation
autophagy.
This
knowledge
may
help
design
future
clinical
tools
improve
cancer
diagnosis
treatment.
Cell Communication and Signaling,
Journal Year:
2023,
Volume and Issue:
21(1)
Published: Nov. 16, 2023
Abstract
Regulated
cell
death
(RCD)
is
a
regulable
that
involves
well-organized
signaling
cascades
and
molecular
mechanisms.
RCD
implicated
in
fundamental
processes
such
as
organ
production
tissue
remodeling,
removing
superfluous
structures
or
cells,
regulating
numbers.
Previous
studies
have
not
been
able
to
reveal
the
complete
mechanisms,
novel
methods
of
are
constantly
being
proposed.
Two
metal
ions,
iron
(Fe)
copper
(Cu)
essential
factors
leading
RCDs
only
induce
ferroptosis
cuproptosis,
respectively
but
also
lead
impairment
eventually
diverse
death.
This
review
summarizes
direct
indirect
mechanisms
by
which
Fe
Cu
impede
growth
various
forms
mediated
these
two
metals.
Moreover,
we
aimed
delineate
interrelationships
between
with
distinct
pathways
shedding
light
on
complex
intricate
govern
cellular
survival
Finally,
prospects
outlined
this
suggest
approach
for
investigating
death,
may
involve
integrating
current
therapeutic
strategies
offer
promising
solution
overcome
drug
resistance
certain
diseases.
Advanced Science,
Journal Year:
2024,
Volume and Issue:
11(18)
Published: March 2, 2024
Abstract
The
induction
of
cuproptosis,
a
recently
identified
form
copper‐dependent
immunogenic
cell
death,
is
promising
approach
for
antitumor
therapy.
However,
sufficient
accumulation
intracellular
copper
ions
(Cu
2+
)
in
tumor
cells
essential
inducing
cuproptosis.
Herein,
an
intelligent
cuproptosis‐inducing
nanosystem
constructed
by
encapsulating
oxide
(CuO)
nanoparticles
with
the
ionophore
elesclomol
(ES).
After
uptake
cells,
ES@CuO
degraded
to
release
Cu
and
ES
synergistically
trigger
thereby
significantly
inhibiting
growth
murine
B16
melanoma
cells.
Moreover,
further
promoted
cuproptosis‐mediated
immune
responses
reprogrammed
immunosuppressive
microenvironment
increasing
number
tumor‐infiltrating
lymphocytes
secreted
inflammatory
cytokines.
Additionally,
combining
programmed
death‐1
(PD‐1)
immunotherapy
substantially
increased
efficacy
melanoma.
Overall,
findings
this
study
can
lead
use
novel
strategy
therapy,
which
may
enhance
checkpoint
inhibitor
Current Medical Science,
Journal Year:
2024,
Volume and Issue:
44(1), P. 28 - 50
Published: Feb. 1, 2024
Abstract
Copper
is
an
essential
trace
element,
and
plays
a
vital
role
in
numerous
physiological
processes
within
the
human
body.
During
normal
metabolism,
body
maintains
copper
homeostasis.
deficiency
or
excess
can
adversely
affect
cellular
function.
Therefore,
homeostasis
stringently
regulated.
Recent
studies
suggest
that
trigger
specific
form
of
cell
death,
namely,
cuproptosis,
which
triggered
by
excessive
levels
intracellular
copper.
Cuproptosis
induces
aggregation
mitochondrial
lipoylated
proteins,
loss
iron-sulfur
cluster
proteins.
In
neurodegenerative
diseases,
pathogenesis
progression
neurological
disorders
are
linked
to
This
review
summarizes
advances
cuproptosis
nervous
system
diseases.
offers
research
perspectives
provide
new
insights
into
targeted
treatment
diseases
based
on
cuproptosis.
Cell Communication and Signaling,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: July 5, 2024
Abstract
Copper
is
a
crucial
trace
element
that
plays
role
in
various
pathophysiological
processes
the
human
body.
also
acts
as
transition
metal
involved
redox
reactions,
contributing
to
generation
of
reactive
oxygen
species
(ROS).
Under
prolonged
and
increased
ROS
levels,
oxidative
stress
occurs,
which
has
been
implicated
different
types
regulated
cell
death.
The
recent
discovery
cuproptosis,
copper-dependent
death
pathway
distinct
from
other
known
forms,
raised
interest
researchers
field
cancer
therapy.
Herein,
present
work
aims
outline
current
understanding
with
an
emphasis
on
its
anticancer
activities
through
interplay
copper-induced
stress,
thereby
providing
new
ideas
for
therapeutic
approaches
targeting
modes
future.
Journal of Hematology & Oncology,
Journal Year:
2024,
Volume and Issue:
17(1)
Published: Aug. 16, 2024
Cuproptosis
is
a
newly
identified
form
of
cell
death
induced
by
excessive
copper
(Cu)
accumulation
within
cells.
Mechanistically,
cuproptosis
results
from
Cu-induced
aggregation
dihydrolipoamide
S-acetyltransferase,
correlated
with
the
mitochondrial
tricarboxylic
acid
cycle
and
loss
iron–sulfur
cluster
proteins,
ultimately
resulting
in
proteotoxic
stress
triggering
death.
Recently,
has
garnered
significant
interest
tumor
research
due
to
its
potential
as
crucial
therapeutic
strategy
against
cancer.
In
this
review,
we
summarized
cellular
molecular
mechanisms
relationship
other
types
Additionally,
reviewed
current
drugs
or
strategies
available
induce
cells,
including
Cu
ionophores,
small
compounds,
nanomedicine.
Furthermore,
targeted
metabolism
specific
regulatory
genes
cancer
therapy
enhance
sensitivity
cuproptosis.
Finally,
discussed
feasibility
targeting
overcome
chemotherapy
immunotherapy
resistance
suggested
future
directions.
This
study
that
could
open
new
avenues
for
developing
therapy.
Frontiers in Cardiovascular Medicine,
Journal Year:
2022,
Volume and Issue:
9
Published: Nov. 11, 2022
Acute
myocardial
infarction
(AMI)
has
the
characteristics
of
sudden
onset,
rapid
progression,
poor
prognosis,
and
so
on.
Therefore,
it
is
urgent
to
identify
diagnostic
prognostic
biomarkers
for
it.
Cuproptosis
a
new
form
mitochondrial
respiratory-dependent
cell
death.
However,
studies
are
limited
on
clinical
significance
cuproptosis-related
genes
(CRGs)
in
AMI.
In
this
study,
we
systematically
assessed
genetic
alterations
CRGs
AMI
by
bioinformatics
approach.
The
results
showed
that
six
(LIAS,
LIPT1,
DLAT,
PDHB,
MTF1,
GLS)
were
markedly
differentially
expressed
between
stable
coronary
heart
disease
(stable_CAD)
Correlation
analysis
indicated
closely
correlated
with
N6-methyladenosine
(m6A)-related
through
R
language
"corrplot"
package,
especially
GLS
was
positively
FMR1
MTF1
negatively
HNRNPA2B1.
Immune
landscape
revealed
related
various
immune
cells,
T
cells
CD4
memory
resting
monocytes.
Kaplan-Meier
demonstrated
group
high
DLAT
expression
had
better
prognosis.
area
under
curve
(AUC)
certified
good
value,
training
set
(AUC
=
0.87)
verification
(ACU
0.99).
Gene
enrichment
(GSEA)
suggested
associated
immune-
hypoxia-related
pathways.
addition,
Ontology
(GO)
analysis,
Kyoto
Encyclopedia
Genes
Genomes
(KEGG)
competing
endogenous
RNA
(ceRNA)
transcription
factor
(TF),
compound
prediction
performed
reveal
regulatory
mechanism
Overall,
our
study
can
provide
additional
information
understanding
role
AMI,
which
may
insights
into
identification
therapeutic
targets
