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.
Nature Communications,
Journal Year:
2024,
Volume and Issue:
15(1)
Published: April 15, 2024
Abstract
Simultaneously
quantifying
mitochondrial
Cu
+
and
2+
levels
is
crucial
for
evaluating
the
molecular
mechanisms
of
copper
accumulation-involved
pathological
processes.
Here,
a
series
molecules
containing
various
diacetylene
derivatives
as
Raman
reporters
are
designed
synthesized,
alkyne-tagged
SERS
probe
created
determination
with
high
selectivity
sensitivity.
The
developed
generates
well-separated
distinguishable
fingerprint
peaks
built-in
corrections
in
cellular
silent
region,
resulting
accurate
quantification
.
present
demonstrates
tempo-spatial
resolution
real-time
imaging
simultaneously
long-term
stability
benefiting
from
assembly
Au-C≡C
groups.
Using
this
powerful
tool,
it
found
that
increase
during
ischemia
associated
breakdown
proteins
well
conversion
Meanwhile,
we
observe
parts
transported
out
neurons
by
ATPase.
More
importantly,
cuproptosis
including
oxidative
stress
process
caused
to
,
which
dominates
at
early
stage
(<9
h),
subsequent
proteotoxic
stress.
Both
stresses
contribute
neuronal
death.
Journal of Translational Medicine,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: Jan. 22, 2025
Cuproptosis
differs
from
other
forms
of
cell
death,
such
as
apoptosis,
necroptosis,
and
ferroptosis,
in
its
unique
molecular
mechanisms
signaling
pathways.
In
this
review,
we
delve
into
the
cellular
metabolic
pathways
copper,
highlighting
role
copper
biomolecule
synthesis,
mitochondrial
respiration,
antioxidant
defense.
Furthermore,
elucidate
relationship
between
cuproptosis-related
genes
(CRGs)
cancer
prognosis,
analyzing
their
expression
patterns
across
various
tumor
types
impact
on
patient
outcomes.
Our
review
also
uncovers
potential
therapeutic
applications
chelators,
ionophores,
copper-based
nanomaterials
oncology.
addition,
discuss
emerging
cuproptosis
remodeling
microenvironment,
enhancing
immune
infiltration,
converting
"cold
tumors"
"hot
that
respond
better
to
immunotherapy.
short,
underscores
pivotal
importance
biology
highlights
translational
a
novel
target.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(21), P. 15721 - 15721
Published: Oct. 29, 2023
Trace
elements
and
metals
play
critical
roles
in
the
normal
functioning
of
central
nervous
system
(CNS),
their
dysregulation
has
been
implicated
neurodegenerative
disorders
such
as
Alzheimer’s
disease
(AD)
Parkinson’s
(PD).
In
a
healthy
CNS,
zinc,
copper,
iron,
manganese
vital
enzyme
cofactors,
supporting
neurotransmission,
cellular
metabolism,
antioxidant
defense.
Imbalances
these
trace
can
lead
to
oxidative
stress,
protein
aggregation,
mitochondrial
dysfunction,
thereby
contributing
neurodegeneration.
AD,
copper
zinc
imbalances
are
associated
with
amyloid-beta
tau
pathology,
impacting
cognitive
function.
PD
involves
disruption
iron
levels,
leading
damage
neuronal
loss.
Toxic
metals,
like
cadmium,
impair
synaptic
transmission
exacerbate
neuroinflammation,
CNS
health.
The
role
aluminum
AD
neurofibrillary
tangle
formation
also
noted.
Understanding
health
might
offer
potential
therapeutic
targets
for
disorders.
Codex
Alimentarius
standards
concerning
mentioned
foods
may
be
one
key
legal
contributions
safeguarding
public
Further
research
is
needed
fully
comprehend
complex
mechanisms
develop
effective
interventions.
ACS Sensors,
Journal Year:
2024,
Volume and Issue:
9(6), P. 2858 - 2868
Published: May 24, 2024
Copper
participates
in
a
range
of
critical
functions
the
nervous
system
and
human
brain.
Disturbances
brain
copper
content
is
strongly
associated
with
neurological
diseases.
For
example,
changes
level
distribution
are
reported
neuroblastoma,
Alzheimer's
disease,
Lewy
body
disorders,
such
as
Parkinson
disease
dementia
bodies
(DLB).
There
need
for
more
sensitive
techniques
to
measure
intracellular
levels
have
better
understanding
role
homeostasis
neuronal
disorders.
Here,
we
report
reaction-based
near-infrared
(NIR)
ratiometric
fluorescent
probe
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(6), P. 3248 - 3248
Published: March 13, 2024
Mast
cells
(MCs)
are
derived
from
hematopoietic
progenitors,
mature
in
vascularized
tissues,
and
participate
innate
acquired
immunity.
Neuroinflammation
is
a
highly
debated
topic
the
biomedical
literature;
however,
impact
of
tumor
necrosis
factor
(TNF)
IL-33
on
MCs
brain
has
not
been
widely
addressed.
can
be
activated
by
IgE
binding
to
FcεRI,
as
well
different
antigens.
After
activation,
mediate
various
immunological
inflammatory
responses
through
TNF
IL-33.
two
receptors:
TNFR1,
p55
molecule,
TNFR2,
p75
molecule.
This
cytokine
only
one
its
kind
stored
granules
also
generated
de
novo
synthesis
via
mRNA.
In
central
nervous
system
(CNS),
produced
almost
exclusively
microglial
cells,
neurons,
astrocytes,
and,
minimally,
endothelial
cells.
release
into
tissue,
rapidly
induces
adhesion
molecules
leukocyte
molecule
1
(ELAM-1),
intercellular
(ICAM-1),
vascular
cell
(VCAM-1)
causes
chemoattraction
neutrophils
inducing
several
molecules,
including
CXC
chemokines
(IL-8).
Both
act
primary
barrier
against
foreign
CNS,
producing
pro-inflammatory
cytokines
such
belongs
IL-1
family,
ST2L/IL1-RAcP
receptor
complex,
mediates
both
adaptive
immune
response.
nuclear
transcription
expressed
brain,
where
it
(TNF
IL-1)
(CCL2,
CCL3,
CCL5,
CXCL10).
Therefore,
microglia
CNS
source
cytokines,
IL-33,
that
many
diseases.
The
inhibition
may
represent
new
therapeutic
approach
could
complement
existing
neuroinflammatory
therapies.
Redox Biology,
Journal Year:
2024,
Volume and Issue:
72, P. 103156 - 103156
Published: April 12, 2024
Regulation
of
the
oxidative
stress
response
is
crucial
for
management
and
prognosis
traumatic
brain
injury
(TBI).
The
copper
chaperone
Antioxidant
1
(Atox1)
plays
a
role
in
regulating
intracellular
ion
balance
impacting
antioxidant
capacity
mitochondria,
as
well
state
cells.
However,
it
remains
unknown
whether
Atox1
involved
modulating
following
TBI.
Here,
we
investigated
regulatory
on
neurons
both
vivo
vitro,
elucidated
underlying
mechanism
through
culturing
hippocampal
HT-22
cells
with
mutation.
expression
was
significantly
diminished
TBI,
while
mice
overexpressed
exhibited
more
preserved
structure
reduced
levels
post-TBI.
Furthermore,
displayed
notable
impairments
learning
memory
functions
after
which
were
ameliorated
by
overexpression
Atox1.
In
stretch
model
cells,
mitigated
preserving
normal
morphology
network
connectivity
facilitating
elimination
damaged
mitochondria.
Mechanistically,
co-immunoprecipitation
mass
spectrometry
revealed
binding
to
DJ-1.
Knockdown
DJ-1
impaired
Mutations
copper-binding
motif
or
sequestration
free
led
substantial
decrease
interaction
between
DJ-1,
failing
restore
mutants.
findings
suggest
that
mediates
ability
withstand
stress.
And
targeting
could
be
potential
therapeutic
approach
addressing
post-traumatic
neurological
dysfunction.
Frontiers in Molecular Biosciences,
Journal Year:
2024,
Volume and Issue:
11
Published: Feb. 8, 2024
Copper
(Cu)
is
an
essential
trace
element,
however
excess
toxic
due
to
its
redox
properties.
Cu
homeostasis
therefore
needs
be
tightly
regulated
via
cellular
transporters,
storage
proteins
and
exporters.
An
imbalance
in
has
been
associated
with
neurodegenerative
disorders
such
as
Wilson’s
disease,
but
also
Alzheimer’s
or
Parkinson’s
disease.
In
our
current
study,
we
explored
the
utility
of
using
Caenorhabditis
elegans
(
C.
)
a
model
dyshomeostasis.
The
application
dosing
use
mutants
lacking
intracellular
chaperone
atox-1
major
protein
ceruloplasmin
facilitated
assessment
status,
functional
markers
including
total
levels,
labile
distribution
gene
expression
homeostasis-related
genes.
Our
data
revealed
decrease
uptake
increase
levels
genetic
dysfunction,
well
altered
homeostasis-associated
addition,
uncovered
role
play
worm’s
homeostasis.
This
study
provides
insights
into
suitable
,
focus
on
promising
marker
dysregulation
during
disease
progression.
Clinical and Experimental Medicine,
Journal Year:
2024,
Volume and Issue:
24(1)
Published: Sept. 26, 2024
Abstract
Long
non-coding
RNAs
(lncRNAs)
have
emerged
as
crucial
regulators
in
various
cellular
processes,
including
cancer
progression
and
stress
response.
Recent
studies
demonstrated
that
copper
accumulation
induces
a
unique
form
of
cell
death
known
cuproptosis,
with
lncRNAs
playing
key
role
regulating
cuproptosis-associated
pathways.
These
may
trigger
cell-specific
responses
to
stress,
presenting
new
opportunities
prognostic
markers
therapeutic
targets.
This
paper
delves
into
the
cuproptosis-mediated
cancer,
underscoring
their
potential
biomarkers
targets
for
innovative
strategies.
A
thorough
review
scientific
literature
was
conducted,
utilizing
databases
such
PubMed,
Google
Scholar,
ScienceDirect,
search
terms
like
'lncRNAs,'
'cuproptosis,'
'cancer.'
Studies
were
selected
based
on
relevance
lncRNA
regulation
cuproptosis
pathways
implications
prognosis
treatment.
The
highlights
significant
contribution
cuproptosis-related
genes
pathways,
impacting
metabolism,
mitochondrial
responses,
apoptotic
signaling.
Specific
are
breast,
lung,
liver,
ovarian,
pancreatic,
gastric
cancers.
objective
this
article
is
explore
cancers
mediated
by
cuproptosis.
