Copper in melanoma: at the crossroad of protumorigenic and anticancer roles
Natalia Chrzan,
No information about this author
Mariusz L. Hartman
No information about this author
Redox Biology,
Journal Year:
2025,
Volume and Issue:
81, P. 103552 - 103552
Published: Feb. 15, 2025
Language: Английский
Nanomaterial‐Triggered Ferroptosis and Cuproptosis in Cancer Therapy
Small,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 28, 2025
Abstract
Cancer
remains
one
of
the
leading
causes
death
individuals
globally.
Conventional
treatment
techniques
like
chemotherapy
and
radiation
often
suffer
various
drawbacks
toxicity
drug
resistance.
The
study
cell
has
been
predominantly
focused
on
classical
forms
apoptosis,
but
role
metal
ions
in
governing
controlled
is
a
fascinating
less
explored
area.
Metal‐mediated
process
where
triggers
via
unique
mechanism.
Nanomaterial‐based
strategies
have
gained
attention
for
their
ability
to
deliver
precise
therapeutic
agents
while
also
triggering
Regulated
Cell
Death
(RCD)
mechanisms
cancer
cells.
recently
discovered
metal‐mediated
cuproptosis
ferroptosis
can
be
used
as
they
selectively
drug‐resistant
cancer.
Nano
material‐based
delivery
system
targeted
sites.
In
this
review,
we
given
some
idea
about
mechanism
(ferroptosis
cuproptosis)
how
initiate
deaths
using
nanomaterials
treatment.
Language: Английский
Editorial: Targeting the aging mitochondria: mechanisms, methods, and therapeutic strategies
Frontiers in Aging Neuroscience,
Journal Year:
2025,
Volume and Issue:
17
Published: March 27, 2025
Figure
1.
The
Mitochondrial
Path:
From
Mechanisms
to
Therapeutics.
Several
mitochondria-targeted
approaches
show
promise
for
promoting
healthy
brain
aging,
combating
neurodegeneration,
and
addressing
reproductive
aging.
This
research
topic
highlights
a
new
form
of
mitochondria-associated
programmed
cell
death
called
cuproptosis,
the
master
regulator
mitochondrial
biogenesis
PGC-1α,
oxidative
stress
responses
where
FOXO
transcription
factors
play
pivotal
role
in
homeostasis.Synaptic
plasticity
is
fundamental
preserving
function.
deficits,
particularly
those
affecting
organelle
distribution,
motility,
calcium
buffering
capacity,
have
been
associated
with
impairments
synaptic
transmission,
potentiation,
(Todorova
Blokland
2017).
Navakkode
Kennedy
highlight
importance
assessing
cognition
alongside
physical
fitness
lifespan
aging
studies.
Importantly,
cognitive
decline
not
an
inevitable
consequence
but
rather
process
shaped
by
genetic,
environmental,
lifestyle
factors.
Maintaining
functions
reserves
identifying
key
molecular
drivers
resilience
enhancing
neuroplasticity
(possibly
through
interventions)
could
provide
proactive
strategy
function
populations.In
neurological
health,
mitochondria
also
death,
like
apoptosis,
mitophagy-associated
pyroptosis,
necroptosis,
ferroptosis,
cuproptosis
(Zhu,
Song
et
al.
2024).
Cuproptosis
has
identified
as
novel
copper-dependent
mitochondria-mediated
(Tsvetkov,
Coy
2022,
Wang,
Zhang
2022).
Fan
emphasize
that
this
emerging
concept
adds
dimension
understanding
age-related
diseases.
While
copper
essential
enzymatic
cellular
homeostasis,
its
dysregulation
can
lead
protein
aggregation
cytotoxicity,
exacerbating
neurodegeneration
systemic
In
future,
potential
therapeutic
targets
mitigating
pathologies,
underscoring
precision
medicine
research.Mitochondrial
are
largely
coordinated
peroxisome
proliferator-activated
receptor-γ
coactivator-1α
(PGC-1α),
common
feature
many
diseases
(Panes,
Wendt
Its
biosynthesis
metabolic
regulation
maintenance
neuronal
integrity.
Tang
describe
PGC-1α
protective
factor
against
neuroinflammation,
stress,
autophagy-related
dysfunction
conditions
such
Alzheimer's
disease,
Parkinson's
amyotrophic
lateral
sclerosis.
They
discuss
various
compounds
drug-targeting
strategies
may
ameliorate
these
pathologies.
As
our
deepens,
targeting
offer
promising
avenues
improving
health
slowing
or
even
preventing
neurodegeneration.
Future
studies
should
focus
on
optimizing
modulation
enhance
effects
while
minimizing
off-target
consequences.The
regulatory
hub
plays
protecting
cells
from
stress.
excessive
reactive
oxygen
species
(ROS)
generation
closely
linked
Notably,
recent
study
emphasizes
target,
OSER1,
which
helps
withstand
(Song,
Li
underscore
critical
redox
balance
maintaining
germ
fertility.
Given
mitochondria's
energy
production
pathways
reduce
extend
both
men
women.
interplay
between
damage
creates
cycle
accelerates
declines
Understanding
mechanisms
crucial
developing
effective
therapies
address
infertility.
intersection
longevity
remains
compelling
frontier
agingrelated
research.The
convergence
multifaceted
nature
need
holistic
approach
mitigation.
integrity,
regulation,
metal
ion
adaptability
interconnected
influence
at
multiple
levels.
By
integrating
insights
neurology,
biology,
research,
scientists
clinicians
develop
more
mitochondrialtargeted
interventions
healthspan.As
we
continue
unravel
presents
delaying
neurodegenerative
diseases,
decline,
health.
challenge
now
lies
translating
groundbreaking
discoveries
into
tangible
promote
Language: Английский
Molecular mechanisms of alcohol-associated liver disease-ferroptosis and autophagy crosstalk
Yangyang Wang,
No information about this author
Xin Zhou,
No information about this author
Hui Chen
No information about this author
et al.
Molecular Biology Reports,
Journal Year:
2025,
Volume and Issue:
52(1)
Published: April 4, 2025
Language: Английский
Cuproptosis and its potential role in musculoskeletal disease
Frontiers in Cell and Developmental Biology,
Journal Year:
2025,
Volume and Issue:
13
Published: April 11, 2025
Cuproptosis,
a
recently
identified
form
of
copper-dependent
cell
death,
arises
from
intracellular
copper
dyshomeostasis.
As
an
essential
trace
element,
plays
critical
role
in
bioenergetic
metabolism,
redox
regulation,
and
synaptic
transmission.
However,
excessive
exerts
cytotoxic
effects
through
multiple
pathways,
including
increased
reactive
oxygen
species
(ROS)
production,
apoptotic
cascade
activation,
necrotic
membrane
rupture,
inflammatory
responses,
mitochondrial
dysfunction.
Distinct
other
death
mechanisms,
cuproptosis
is
characterized
by
ion
binding
to
acetylated
respiratory
chain
proteins,
leading
pathogenic
protein
aggregation,
iron-sulfur
cluster
depletion,
cellular
collapse.
Emerging
evidence
underscores
aberrant
accumulation
resultant
proteotoxic
stress
as
pivotal
contributors
the
pathogenesis
musculoskeletal
pathologies,
osteoporosis,
osteoarthritis,
sarcopenia,
osteosarcoma,
intervertebral
disc
degeneration,
spinal
cord
injury,
biofilm-associated
orthopedic
infections.
Understanding
spatiotemporal
regulation
may
provide
novel
opportunities
for
advancing
diagnostic
therapeutic
approaches
medicine.
This
review
synthesizes
current
insights
into
molecular
mechanisms
cuproptosis,
its
diseases,
potential
biomarker-driven
interventions.
Language: Английский