Cell Biology and Toxicology,
Journal Year:
2024,
Volume and Issue:
40(1)
Published: July 29, 2024
Abstract
Advancements
in
the
CRISPR
technology,
a
game-changer
experimental
research,
have
revolutionized
various
fields
of
life
sciences
and
more
profoundly,
cancer
research.
Cell
death
pathways
are
among
most
deregulated
cells
considered
as
critical
aspects
development.
Through
decades,
our
knowledge
mechanisms
orchestrating
programmed
cellular
has
increased
substantially,
attributed
to
revolution
cutting-edge
technologies.
The
heroic
appearance
systems
expanded
available
screening
platform
genome
engineering
toolbox
detect
mutations
create
precise
edits.
In
that
context,
ability
this
system
for
identification
targeting
cell
signaling
result
development
therapy
resistance
is
an
auspicious
choice
transform
accelerate
individualized
therapy.
concept
personalized
stands
on
molecular
characterization
individual
tumor
its
microenvironment
order
provide
treatment
with
highest
possible
outcome
minimum
toxicity.
This
study
explored
potential
technology
precision
by
identifying
specific
pathways.
It
showed
promise
finding
key
components
involved
death,
making
it
tool
targeted
However,
also
highlighted
challenges
limitations
need
be
addressed
future
research
fully
realize
treatment.
Graphical
abstract
Current
application
through
glance.
A
choosing
appropriate
biological
model
vitro
(using
established
lines,
animal
derived
cells,
human
stem
or
T
cells),
vivo
models
which
can
harbor
tumor),
ex
(human/animal-derived
organoids).
B
preparation
gRNA
library.
C
design
screening,
desired
gRNAs
phenotypic
response.
D
CRISPR-Cas
identified
targets,
Cas9
gene
editing
(Knockout,
base
editing,
prime
editing),
RNA
modulation
(modulation
splicing,
interference),
epigenomic
edits
interference/activation
using
dead
(dCas9)
(Bock
et
al.
2022b)
International Journal of Molecular Sciences,
Journal Year:
2020,
Volume and Issue:
21(22), P. 8765 - 8765
Published: Nov. 20, 2020
Ferroptosis
is
a
type
of
cell
death
that
was
described
less
than
decade
ago.
It
caused
by
the
excess
free
intracellular
iron
leads
to
lipid
(hydro)
peroxidation.
Iron
essential
as
redox
metal
in
several
physiological
functions.
The
brain
one
organs
known
be
affected
homeostatic
balance
disruption.
Since
1960s,
increased
concentration
central
nervous
system
has
been
associated
with
oxidative
stress,
oxidation
proteins
and
lipids,
death.
Here,
we
review
main
mechanisms
involved
process
ferroptosis
such
peroxidation,
glutathione
peroxidase
4
enzyme
activity,
metabolism.
Moreover,
association
pathophysiology
some
neurodegenerative
diseases,
namely
Alzheimer’s,
Parkinson’s,
Huntington’s
also
addressed.
International Journal of Biological Sciences,
Journal Year:
2022,
Volume and Issue:
18(5), P. 1829 - 1843
Published: Jan. 1, 2022
Ferroptosis
is
a
novel
form
of
programmed
cell
death,
and
it
characterized
by
iron-dependent
oxidative
damage,
lipid
peroxidation
reactive
oxygen
species
accumulation.
Notable
studies
have
revealed
that
ferroptosis
plays
vital
roles
in
tumor
occurrence
abundant
cells
can
inhibit
progression.
Recently,
some
noncoding
RNAs
(ncRNAs),
particularly
microRNAs,
long
RNAs,
circular
been
shown
to
be
involved
biological
processes
ferroptosis,
thus
affecting
cancer
growth.
However,
the
definite
regulatory
mechanism
this
phenomenon
still
unclear.
To
clarify
issue,
increasing
focused
on
ncRNAs
initiation
development
role
progression
various
cancers,
such
as
lung,
liver,
breast
cancers.
In
review,
we
systematically
summarized
relationship
between
ferroptosis-associated
Moreover,
additional
evidence
needed
identify
ferroptosis-related
This
review
will
help
us
understand
may
provide
new
ideas
for
exploring
diagnostic
therapeutic
biomarkers
future.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(4), P. 3658 - 3658
Published: Feb. 11, 2023
Senescence
is
a
cellular
aging
process
in
all
multicellular
organisms.
It
characterized
by
decay
functions
and
proliferation,
resulting
increased
damage
death.
This
condition
plays
an
essential
role
the
significantly
contributes
to
development
of
age-related
complications.
On
other
hand,
ferroptosis
systemic
cell
death
pathway
excessive
iron
accumulation
followed
generation
reactive
oxygen
species
(ROS).
Oxidative
stress
common
trigger
this
may
be
induced
various
factors
such
as
toxins,
drugs,
inflammation.
Ferroptosis
linked
numerous
disorders,
including
cardiovascular
disease,
neurodegeneration,
cancer.
believed
contribute
tissue
organ
occurring
with
aging.
has
also
been
pathologies,
diseases,
diabetes,
In
particular,
senescent
cells
have
shown
produce
inflammatory
cytokines
pro-inflammatory
molecules
that
can
these
conditions.
turn,
health
known
play
pathologies
promoting
damaged
or
diseased
contributing
inflammation
often
associated.
Both
senescence
are
complex
pathways
still
not
fully
understood.
Further
research
needed
thoroughly
investigate
processes
identify
potential
interventions
target
order
prevent
treat
systematic
review
aims
assess
mechanisms
underlying
link
connecting
senescence,
ferroptosis,
aging,
whether
they
exploited
block
limit
physiological
elderly
people
for
healthy
longevity.
Cell Death Discovery,
Journal Year:
2024,
Volume and Issue:
10(1)
Published: May 30, 2024
Abstract
Ferroptosis
represents
a
form
of
programmed
cell
death
that
is
propelled
by
iron-dependent
lipid
peroxidation,
thereby
being
distinguished
the
prominent
features
iron
accumulation
and
peroxidation.
has
been
implicated
in
numerous
physiological
pathological
phenomena,
with
mounting
indications
it
holds
significant
implications
for
cancer
other
medical
conditions.
On
one
side,
demonstrates
anti-cancer
properties
triggering
ferroptosis
within
malignant
cells,
on
hand,
damages
normal
cells
causing
diseases.
Therefore,
this
paper,
we
propose
to
review
paradoxical
regulation
tumors
First,
introduce
development
history,
concept
mechanism
ferroptosis.
The
second
part
focuses
methods
inducing
tumors.
third
section
emphasizes
utilization
different
conditions
strategies
inhibit
fourth
elucidates
key
contradictions
control
Finally,
potential
research
avenues
associated
domains
are
suggested.
Cells,
Journal Year:
2025,
Volume and Issue:
14(7), P. 511 - 511
Published: March 29, 2025
Oxidative
stress
(OS)
is
an
established
hallmark
of
cancer
and
neurodegenerative
disorders
(NDDs),
which
contributes
to
genomic
instability
neuronal
loss.
This
review
explores
the
contrasting
role
OS
in
stem
cells
(CSCs)
NDDs.
Elevated
levels
reactive
oxygen
species
(ROS)
contribute
promote
tumor
initiation
progression
CSCs,
while
NDDs
such
as
Alzheimer’s
Parkinson’s
disease,
accelerates
death
impairs
cellular
repair
mechanisms.
Both
scenarios
involve
disruption
delicate
balance
between
pro-oxidant
antioxidant
systems,
leads
chronic
oxidative
stress.
Notably,
CSCs
neurons
display
alterations
redox-sensitive
signaling
pathways,
including
Nrf2
NF-κB,
influence
cell
survival,
proliferation,
differentiation.
Mitochondrial
dynamics
further
illustrate
these
differences:
enhanced
function
supports
adaptability
whereas
impairments
heighten
vulnerability.
Understanding
common
mechanisms
OS-induced
redox
imbalance
may
provide
insights
for
developing
interventions,
addressing
aging
hallmarks,
potentially
mitigating
or
preventing
both
