Medicine,
Год журнала:
2023,
Номер
102(48), С. e36375 - e36375
Опубликована: Дек. 1, 2023
Cognitive
dysfunction
occurs
mainly
in
certain
diseases
and
the
pathological
process
of
aging.
In
addition
to
this,
it
is
also
widespread
patients
undergoing
anesthesia,
surgery,
cancer
chemotherapy.
Neuroinflammation,
oxidative
stress,
mitochondrial
dysfunction,
impaired
synaptic
plasticity,
lack
neurotrophic
support
are
involved
copper-induced
cognitive
dysfunction.
addition,
recent
studies
have
found
that
copper
mediates
cuproptosis
adversely
affects
function.
Cuproptosis
a
copper-dependent,
lipoylated
protein-driven,
non-apoptotic
mode
regulated
cell
death,
which
provides
us
with
new
avenues
for
identifying
treating
related
diseases.
However,
exact
mechanism
by
induces
decline
still
unclear,
this
has
attracted
interest
many
researchers.
paper,
we
analyzed
mechanisms
therapeutic
targets
copper-associated
decline,
context
neurodegenerative
diseases,
psychiatric
psychological
disorders,
diabetes
mellitus.
Cancer Cell International,
Год журнала:
2025,
Номер
25(1)
Опубликована: Апрель 9, 2025
Hepatocellular
carcinoma
(HCC)
is
the
main
phenotype
of
liver
cancer
with
a
poor
prognosis.
Copper
vital
in
function,
and
HCC
cells
rely
on
it
for
growth
metastasis,
leading
to
cuproplasia.
Excessive
copper
can
induce
cell
death,
termed
cuproptosis.
Tumor
microenvironment
(TME)
pivotal
HCC,
especially
immunotherapy,
closely
related
TME
pathogenesis.
However,
how
these
two
mechanisms
contribute
intriguing.
We
conducted
latest
progress
literature
cuproplasia
cuproptosis
summarized
their
specific
roles
treatment
strategies.
The
relationship
role
have
been
deeply
summarized.
Cuproplasia
fosters
formation,
angiogenesis,
whereas
may
alleviate
mitochondrial
dysfunction
hypoxic
conditions
TME.
Inhibiting
enhancing
are
essential
achieving
therapeutic
efficacy
HCC.
An
in-depth
analysis
within
unveils
opposing
nature
impact
regulation.
Grasping
equilibrium
between
factors
crucial
deeper
understanding
shed
light
novel
directions
treating
Scientific Reports,
Год журнала:
2023,
Номер
13(1)
Опубликована: Сен. 11, 2023
Abstract
Ferroptosis
is
a
form
of
regulated
cell
death
characterized
by
oxidative
injury-induced
lipid
peroxidation.
However,
the
detailed
protein
post-translational
modification
regulatory
mechanism
ferroptosis
remains
largely
unknown.
Here,
we
report
that
E1A
binding
P300
(EP300)
acetyltransferase
promotes
in
human
pancreatic
ductal
adenocarcinoma
(PDAC)
cells
via
acetylation
heat
shock
family
A
(Hsp70)
member
5
(HSPA5),
also
known
as
GRP78
or
BIP)
on
site
K353.
Acetylated
HSPA5
loses
its
ability
to
inhibit
peroxidation
and
subsequent
ferroptotic
death.
Genetic
pharmacological
inhibition
EP300-mediated
K353
increases
PDAC
resistance
ferroptosis.
Moreover,
histone
deacetylase
6
(HDAC6)
limits
Collectively,
these
findings
not
only
identify
pathways
for
during
ferroptosis,
but
highlight
promising
strategies
increase
sensitivity
cells.
Antioxidants and Redox Signaling,
Год журнала:
2023,
Номер
39(7-9), С. 569 - 590
Опубликована: Март 31, 2023
Significance:
As
a
redox-sensitive
protein,
high-mobility
group
box
1
(HMGB1)
is
implicated
in
regulating
stress
responses
to
oxidative
damage
and
cell
death,
which
are
closely
related
the
pathology
of
inflammatory
diseases,
including
cancer.
Recent
Advances:
HMGB1
nonhistone
nuclear
protein
that
acts
as
deoxyribonucleic
acid
chaperone
control
chromosomal
structure
function.
can
also
be
released
into
extracellular
space
function
damage-associated
molecular
pattern
during
apoptosis,
necrosis,
necroptosis,
pyroptosis,
ferroptosis,
alkaliptosis,
cuproptosis.
Once
released,
binds
membrane
receptors
shape
immune
metabolic
responses.
In
addition
subcellular
localization,
activity
depend
on
its
redox
state
posttranslational
modifications.
Abnormal
plays
dual
role
tumorigenesis
anticancer
therapy
(e.g.,
chemotherapy,
radiation
therapy,
immunotherapy)
depending
tumor
types
stages.
Critical
Issues:
A
comprehensive
understanding
cellular
homeostasis
important
for
deciphering
normal
functions
pathological
manifestations.
this
review,
we
discuss
compartmental-defined
roles
death
Understanding
these
advances
may
help
us
develop
potential
HMGB1-targeting
drugs
or
approaches
treat
stress-related
diseases
conditions.
Future
Directions:
Further
studies
required
dissect
mechanism
by
maintains
under
different
multidisciplinary
effort
evaluate
applications
precisely
targeting
pathway
human
health
disease.
Antioxid.
Redox
Signal.
39,
569-590.
Medicine,
Год журнала:
2023,
Номер
102(48), С. e36375 - e36375
Опубликована: Дек. 1, 2023
Cognitive
dysfunction
occurs
mainly
in
certain
diseases
and
the
pathological
process
of
aging.
In
addition
to
this,
it
is
also
widespread
patients
undergoing
anesthesia,
surgery,
cancer
chemotherapy.
Neuroinflammation,
oxidative
stress,
mitochondrial
dysfunction,
impaired
synaptic
plasticity,
lack
neurotrophic
support
are
involved
copper-induced
cognitive
dysfunction.
addition,
recent
studies
have
found
that
copper
mediates
cuproptosis
adversely
affects
function.
Cuproptosis
a
copper-dependent,
lipoylated
protein-driven,
non-apoptotic
mode
regulated
cell
death,
which
provides
us
with
new
avenues
for
identifying
treating
related
diseases.
However,
exact
mechanism
by
induces
decline
still
unclear,
this
has
attracted
interest
many
researchers.
paper,
we
analyzed
mechanisms
therapeutic
targets
copper-associated
decline,
context
neurodegenerative
diseases,
psychiatric
psychological
disorders,
diabetes
mellitus.
