Advanced Healthcare Materials,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Nov. 5, 2024
Abstract
Nanomedicine
has
shown
great
anticancer
potential
by
disrupting
redox
homeostasis
and
increasing
the
levels
of
oxidative
stress,
but
therapeutic
effect
is
limited
factors
including
intrinsic
self‐protection
mechanism
tumors.
Cancer
cell
death
can
be
induced
exploration
different
mechanisms,
such
as
apoptosis,
pyroptosis,
necroptosis,
cuproptosis,
ferroptosis.
The
merging
nanotechnology
with
biomedicine
provided
tremendous
opportunities
to
construct
death‐based
nanomedicine
for
innovative
cancer
therapy.
Nanocarriers
are
not
only
used
targeted
delivery
inducers,
also
components
induce
achieve
efficient
tumor
treatment.
This
review
focuses
on
seven
modalities
mediated
nanomaterials,
ferroptosis,
cuprotosis,
immunogenic
death,
autophagy.
mechanisms
these
described
in
detail,
well
preparation
nanomaterials
that
them
they
exert
their
effects.
Finally,
this
work
describes
future
development
based
current
knowledge
related
nanomaterials.
Nature Communications,
Journal Year:
2024,
Volume and Issue:
15(1)
Published: May 7, 2024
Abstract
Sleep
disorders
increase
the
risk
and
mortality
of
heart
disease,
but
brain-heart
interaction
has
not
yet
been
fully
elucidated.
Cuproptosis
is
a
copper-dependent
type
cell
death
activated
by
excessive
accumulation
intracellular
copper.
Here,
we
showed
that
16
weeks
sleep
fragmentation
(SF)
resulted
in
elevated
copper
levels
male
mouse
exacerbated
myocardial
ischemia–reperfusion
injury
with
increased
cuproptosis
apoptosis.
Mechanistically,
found
SF
promotes
sympathetic
overactivity,
increases
germination
nerve
terminals,
level
norepinephrine
cardiac
tissue,
thereby
inhibits
VPS35
expression
leads
to
impaired
ATP7A
related
transport
overload
cardiomyocytes.
Copper
further
apoptosis,
these
effects
can
be
rescued
excision
or
administration
chelating
agent.
Our
study
elucidates
one
molecular
mechanisms
which
aggravate
suggests
possible
targets
for
intervention.
Poultry Science,
Journal Year:
2024,
Volume and Issue:
103(9), P. 104011 - 104011
Published: June 22, 2024
Exposure
to
copper
(Cu)
has
been
associated
with
metabolic
disorders
in
animals
and
humans,
but
the
underlying
mechanism
remains
unclear.
One-day-old
broiler
chickens,
numbering
a
total
of
192,
were
nourished
dietary
intakes
that
contained
varying
concentrations
Cu,
specifically
11,
110,
220,
330
mg/kg
for
period
extending
over
duration
7
wk.
As
result
study,
Cu
exposure
resulted
vacuolization,
fragmentation
mitochondria
cristae,
increase
autophagosomes
hepatocytes.
Metabolomics
analysis
illustrated
caused
59
different
metabolites
liver,
predominantly
glycerophospholipid
pathway,
leading
disruption.
Moreover,
high-Cu
diet
markedly
reduced
levels
AMPKα1,
p-AMPKα1,
mTOR,
p-mTOR
enhanced
expression
autophagy-related
factors
(Atg5,
Dynein,
Beclin1,
LC3-II).
Overall,
chicken
liver
injury
disturbed
processes
mediated
autophagy
primarily
through
AMPK-mTOR
axis.
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.
Acta Pharmaceutica Sinica B,
Journal Year:
2024,
Volume and Issue:
14(7), P. 2815 - 2853
Published: April 24, 2024
Regulated
cell
death
(RCD)
is
a
controlled
form
of
orchestrated
by
one
or
more
cascading
signaling
pathways,
making
it
amenable
to
pharmacological
intervention.
RCD
subroutines
can
be
categorized
as
apoptotic
non-apoptotic
and
play
essential
roles
in
maintaining
homeostasis,
facilitating
development,
modulating
immunity.
Accumulating
evidence
has
recently
revealed
that
evasion
frequently
the
primary
cause
tumor
survival.
Several
have
garnered
attention
promising
cancer
therapies
due
their
ability
induce
regression
prevent
relapse,
comparable
apoptosis.
Moreover,
they
offer
potential
solutions
for
overcoming
acquired
resistance
tumors
toward
drugs.
With
an
increasing
understanding
underlying
mechanisms
governing
these
subroutines,
growing
number
small-molecule
compounds
targeting
single
multiple
pathways
been
discovered,
providing
novel
strategies
current
therapy.
In
this
review,
we
comprehensively
summarized
regulatory
emerging
mainly
including
autophagy-dependent
death,
ferroptosis,
cuproptosis,
disulfidptosis,
necroptosis,
pyroptosis,
alkaliptosis,
oxeiptosis,
parthanatos,
mitochondrial
permeability
transition
(MPT)-driven
necrosis,
entotic
NETotic
lysosome-dependent
immunogenic
(ICD).
Furthermore,
focused
on
discussing
related
compounds.
brief,
insightful
findings
may
provide
valuable
guidance
investigating
individual
collaborative
approaches
towards
different
ultimately
driving
discovery
target
significantly
enhance
future
therapeutics.
