Bibliometric and Graphical Analysis of Ferroptosis and Aging Research: Trends, Gaps, and Future Directions
Pathology - Research and Practice,
Год журнала:
2025,
Номер
unknown, С. 155949 - 155949
Опубликована: Март 1, 2025
Язык: Английский
Disulfidptosis: a novel cell death modality induced by actin cytoskeleton collapse and a promising target for cancer therapeutics
Cell Communication and Signaling,
Год журнала:
2024,
Номер
22(1)
Опубликована: Окт. 11, 2024
Disulfidptosis
is
a
novel
discovered
form
of
programmed
cell
death
(PCD)
that
diverges
from
apoptosis,
necroptosis,
ferroptosis,
and
cuproptosis,
stemming
disulfide
stress-induced
cytoskeletal
collapse.
In
cancer
cells
exhibiting
heightened
expression
the
solute
carrier
family
7
member
11
(SLC7A11),
excessive
cystine
importation
reduction
will
deplete
nicotinamide
adenine
dinucleotide
phosphate
(NADPH)
under
glucose
deprivation,
followed
by
an
increase
in
intracellular
stress
aberrant
bond
formation
within
actin
networks,
ultimately
culminating
collapse
disulfidptosis.
involves
crucial
physiological
processes
eukaryotic
cells,
such
as
uptake,
NADPH
metabolism,
dynamics.
The
Rac1-WRC
pathway-mediated
polymerization
also
implicated
this
due
to
its
contribution
formation.
However,
precise
mechanisms
underlying
disulfidptosis
role
tumors
are
not
well
understood.
This
probably
multifaceted
functionalities
SLC7A11
complexities
downstream
pathways
driving
review
describes
critical
roles
summarizes
recent
research
advancements
potential
Moreover,
less-studied
aspects
newly
process
highlighted
stimulate
further
investigations
field.
Язык: Английский
Decoding the Role of O-GlcNAcylation in Hepatocellular Carcinoma
Biomolecules,
Год журнала:
2024,
Номер
14(8), С. 908 - 908
Опубликована: Июль 25, 2024
Post-translational
modifications
(PTMs)
influence
protein
functionality
by
modulating
stability,
localization,
and
interactions
with
other
molecules,
thereby
controlling
various
cellular
processes.
Common
PTMs
include
phosphorylation,
acetylation,
ubiquitination,
glycosylation,
SUMOylation,
methylation,
sulfation,
nitrosylation.
Among
these
modifications,
O-GlcNAcylation
has
been
shown
to
play
a
critical
role
in
cancer
development
progression,
especially
hepatocellular
carcinoma
(HCC).
This
review
outlines
the
of
progression
HCC.
Moreover,
we
delve
into
underlying
mechanisms
HCC
highlight
compounds
that
target
O-GlcNAc
transferase
(OGT)
O-GlcNAcase
(OGA)
improve
treatment
outcomes.
Understanding
will
offer
insights
potential
therapeutic
strategies
targeting
OGT
OGA,
which
could
for
patients
Язык: Английский
MCM4 potentiates evasion of hepatocellular carcinoma from sorafenib-induced ferroptosis through Nrf2 signaling pathway
International Immunopharmacology,
Год журнала:
2024,
Номер
142, С. 113107 - 113107
Опубликована: Сен. 13, 2024
Язык: Английский
Iberverin Downregulates GPX4 and SLC7A11 to Induce Ferroptotic Cell Death in Hepatocellular Carcinoma Cells
Biomolecules,
Год журнала:
2024,
Номер
14(11), С. 1407 - 1407
Опубликована: Ноя. 5, 2024
Ferroptosis,
a
recently
elucidated
style
of
regulated
cell
death,
has
emerged
as
significant
area
investigation
in
cancer
biology.
Natural
active
compounds
that
have
anti-cancer
effects
are
promising
candidates
for
prevention.
Iberverin,
natural
compound
derived
from
Язык: Английский
Identification of shared important genes associated with ferroptosis across different etiologies of acute lung injury
Scientific Reports,
Год журнала:
2025,
Номер
15(1)
Опубликована: Апрель 19, 2025
Acute
lung
injury
(ALI)
of
different
etiologies
has
shared
pathophysiologic
process,
from
which
we
speculated
that
ALI
may
share
common
molecular
features.
While
the
genetic
characteristics
remain
unclear.
In
this
paper,
aimed
to
identify
ferroptosis-associated
and
bottleneck
genes
acute
etiologies.
Firstly,
extracted
five
groups
gene
sets
related
three
distinct
models
Gene
Expression
Omnibus
(GEO)
database.
Then,
through
utilization
weighted
co-expression
network
analysis
(WGCNA),
identified
3
significant
modules
ascertained
7
co-expressed
affected
by
these
models.
Subsequently,
differential
expression
protein-protein
interaction
for
modules,
Slc7a11
was
identified.
Moreover,
subjected
were
used
via
FerrDb
Finally,
key
confirmed
validated.
addition,
observed
is
both
a
driver
suppressor
in
Interestingly,
found
level
significantly
upregulated
Experimentally,
rat
tissues
using
immunofluorescence
staining
real-time
polymerase
chain
reaction
(qRT-PCR)
assays.
Collectively,
our
findings
complement
exploration
pathogenesis
ALI.
There
are
features
etiology
increased
ALI,
can
improve
understanding
mechanisms
underlying
Язык: Английский
Caspase-independent cell death in lung cancer: from mechanisms to clinical applications
Naunyn-Schmiedeberg s Archives of Pharmacology,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 21, 2025
Abstract
Caspase-independent
cell
death
(CICD)
has
recently
become
a
very
important
mechanism
in
lung
cancer,
particular,
to
overcome
critical
failure
apoptotic
that
is
common
disease
progression
and
treatment
failures.
The
pathways
involved
CICD
span
from
necroptosis,
ferroptosis,
mitochondrial
dysfunction,
autophagy-mediated
death.
Its
potential
therapeutic
applications
have
been
highlighted.
Glutathione
peroxidase
4
(GPX4)
inhibition-driven
ferroptosis
drug
resistance
non-small
cancer
(NSCLC).
In
addition,
necroptosis
involving
RIPK1
RIPK3
causes
tumor
modulation
of
immune
responses
the
microenvironment
(TME).
Mitochondrial
are
for
through
metabolic
redox
homeostasis.
Ferroptosis
amplified
by
reactive
oxygen
species
(ROS)
lipid
peroxidation
cells,
depolarization
induces
oxidative
stress
leads
mitochondria-mediated
autophagy,
or
mitophagy,
results
clearance
damaged
organelles
under
conditions,
while
this
function
also
linked
when
dysregulated.
role
autophagy
regulated
ATG
proteins
PI3K/AKT/mTOR
pathway
dual:
suppress
sensitize
cells
therapy.
A
promising
approach
enhancing
outcomes
involves
targeting
mechanisms
CICD,
including
inducing
SLC7A11
inhibition,
modulating
ROS
generation,
combining
inhibition
with
chemotherapy.
Here,
we
review
molecular
underpinnings
particularly
on
their
transform
treatment.
Язык: Английский
Integrated Analysis of Disulfidptosis-Related Genes Identifies CD2AP as a Potential Therapeutic Target for Hepatocellular Carcinoma
International Journal of Molecular Sciences,
Год журнала:
2025,
Номер
26(9), С. 4454 - 4454
Опубликована: Май 7, 2025
Hepatocellular
carcinoma
(HCC)
is
a
deadly
cancer
with
limited
treatment
options
for
patients
at
advanced
stages.
It
urgent
to
develop
reliable
prognostic
risk
models
and
identify
more
biomarkers
improve
the
clinical
outcomes
of
HCC.
Disulfidptosis
newly
discovered
form
regulated
cell
death
(RCD),
research
on
comprehensive
roles
disulfidptosis-related
genes
(DRGs)
in
HCC
prognosis
development
remains
limited.
In
this
paper,
we
systematically
analyzed
expression
levels
profiles
26
DRGs
samples
from
The
Cancer
Genome
Atlas
(TCGA)
cohort
developed
model
using
seven
hub
DRGs.
independent
value
was
further
validated
external
cohort.
overall
survival
low-risk
group
significantly
longer
than
that
those
high-risk
group.
Subsequently,
protein
level
CD2-associated
(CD2AP)
found
be
highly
expressed
tissues
associated
severity
vitro
experiments
demonstrated
down-regulation
CD2AP
attenuated
proliferation,
migration,
invasion,
epithelial–mesenchymal
transition
(EMT)
abilities
cells.
Taken
together,
our
study
revealed
DRG
may
serve
as
potential
biomarker
offer
support
prediction
Язык: Английский