Frontiers in Immunology,
Год журнала:
2024,
Номер
15
Опубликована: Дек. 12, 2024
Ferroptosis
is
a
novel
form
of
cell
death
characterized
by
unlimited
accumulation
iron-dependent
lipid
peroxides.
It
often
accompanied
disease,
and
the
relationship
between
ferroptosis
immune
cells
regulation
has
been
attracting
increasing
attention.
Initially,
it
was
found
in
cancer
research
that
inhibition
regulatory
T
(Treg)
promotion
CD8+
jointly
promoted
formation
an
immune-tolerant
environment
tumors.
T-cell
subsequently
to
have
immunoregulatory
effects
other
diseases.
As
autoimmune
disease
imbalance,
attracted
attention
for
its
potential
regulating
balance
lupus
nephritis.
This
article
reviews
metabolic
processes
within
different
subsets
nephritis
(LN),
including
follicular
helper
(TFH)
cells,
(Th)17
Th1
Th2
Treg
reveals
these
cellular
metabolisms
not
only
facilitate
imbalance
but
are
also
closely
associated
with
occurrence
ferroptosis.
Consequently,
we
hypothesize
targeting
pathways
could
become
direction
effectively
treating
altering
differentiation
incidence
Redox Biology,
Год журнала:
2024,
Номер
75, С. 103257 - 103257
Опубликована: Июнь 26, 2024
Ferroptosis,
a
lipid
peroxidation-driven
cell
death
program
kept
in
check
by
glutathione
peroxidase
4
and
endogenous
redox
cycles,
promises
access
to
novel
strategies
for
treating
therapy-resistant
cancers.
Chlorido
[N,N'-disalicylidene-1,2-phenylenediamine]iron
(III)
complexes
(SCs)
have
potent
anti-cancer
properties
inducing
ferroptosis,
apoptosis,
or
necroptosis
through
still
poorly
understood
molecular
mechanisms.
Here,
we
show
that
SCs
preferentially
induce
ferroptosis
over
other
programs
triple-negative
breast
cancer
cells
(LC
Biomolecules,
Год журнала:
2024,
Номер
14(12), С. 1552 - 1552
Опубликована: Дек. 5, 2024
Pharmacological
treatment
of
diabetes
mellitus-induced
erectile
dysfunction
(DMED)
has
become
increasingly
challenging
due
to
the
limited
efficacy
phosphodiesterase
type
5
inhibitors
(PDE5i).
As
global
prevalence
DM
continues,
there
is
a
critical
need
for
novel
therapeutic
strategies
address
DMED.
In
our
previous
studies,
we
found
that
Glutathione
peroxidase
4
(GPX4),
ferroptosis
inhibitor,
can
ameliorate
DMED
in
diabetic
rats.
However,
specific
role
GPX4
corpus
cavernosum
smooth
muscle
cells
(CCSMCs)
and
its
regulatory
mechanisms
remain
unclear.
this
study,
established
primary
cultures
CCSMCs
systematically
analyzed
under
high-glucose
conditions.
To
further
elucidate
upstream
pathways
GPX4,
employed
immunoprecipitation
coupled
with
mass
spectrometry
(IP-MS)
identify
potential
interacting
proteins.
Additionally,
co-immunoprecipitation
(Co-IP)
cycloheximide
(CHX)
chase
assays
were
conducted
explore
dynamics
post-translational
stability
GPX4.
Under
conditions,
expression
significantly
downregulated,
leading
an
increase
intracellular
oxidative
stress
heightened
levels
ferroptosis,
accompanied
by
cell
relaxation.
Furthermore,
CHX
assay
revealed
high
glucose
accelerates
protein
degradation
via
ubiquitin–proteasome
pathway.
Subsequent
IP-MS
identified
NEDD4,
E3
ubiquitin
ligase,
as
partner
Further
validation
demonstrated
NEDD4
modulates
ubiquitination
process
thereby
influencing
expression.
conclusion,
key
regulator
through
ubiquitin-mediated
proteasomal
degradation.
These
findings
suggest
targeting
NEDD4-GPX4
axis
alleviate
pathology.
Bioresources and Bioprocessing,
Год журнала:
2024,
Номер
11(1)
Опубликована: Авг. 2, 2024
Abstract
Astaxanthin
biosynthesis
in
Haematococcus
pluvialis
is
driven
by
energy.
However,
the
effect
of
flagella-mediated
energy-consuming
movement
process
on
astaxanthin
accumulation
has
not
been
well
studied.
In
this
study,
profiles
and
NADPH
contents
combination
with
photosynthetic
parameters
or
without
flagella
enabled
pH
shock
were
characterized.
The
results
demonstrated
that
there
was
no
significant
alteration
cell
morphology,
exception
loss
observed
treatment
group.
contrast,
content
removal
groups
62.9%,
62.8%
91.1%
higher
than
control
at
4,
8
12
h,
respectively.
Simultaneously,
increased
Y(II)
decreased
Y(NO)
suggest
cells
lacking
flagellar
may
allocate
more
energy
towards
biosynthesis.
This
finding
verified
analysis,
which
revealed
levels
cells.
These
provide
preliminary
insights
into
underlying
mechanism
reassignment
movement-lacking
International Journal of Biological Sciences,
Год журнала:
2024,
Номер
20(11), С. 4146 - 4161
Опубликована: Янв. 1, 2024
Ferroptosis
has
attracted
extensive
interest
from
cancer
researchers
due
to
its
substantial
potential
as
a
therapeutic
target.
The
role
of
LATS2,
core
component
the
Hippo
pathway
cascade,
in
ferroptosis
initiation
hepatoblastoma
(HB)
not
yet
been
investigated.
Furthermore,
underlying
mechanism
decreased
LATS2
expression
remains
largely
unknown.
In
present
study,
we
demonstrated
HB
and
that
overexpression
inhibits
cell
proliferation
by
inducing
ferroptosis.
Increased
reduced
glycine
cysteine
concentrations
via
ATF4/PSAT1
axis.
Physical
binding
between
YAP1/ATF4
PSAT1
promoter
was
confirmed
through
ChIP‒qPCR.
Moreover,
METTL3
identified
writer
mRNA
m6A
modification
at
specific
site
5'
UTR.
Subsequently,
YTHDF2
recognizes
recruits
CCR4-NOT
complex,
leading
degradation
deadenylation.
summary,
N6-methyladenosine
facilitates
degradation.
Reduced
promotes
progression
inhibiting
YAP1/ATF4/PSAT1
Targeting
is
strategy
for
therapy.
Research Square (Research Square),
Год журнала:
2024,
Номер
unknown
Опубликована: Июль 24, 2024
Abstract
Glioma
is
the
most
aggressive
intracranial
malignancy
and
associated
with
poor
survival
rates
limited
quality
of
life,
impairing
neuropsychological
function
cognitive
competence
in
survivors.
The
Proteasome
Subunit
Alpha
Type-5
(PSMA5)
a
multicatalytic
proteinase
complex
that
has
been
linked
tumor
progression
but
rarely
reported
glioma.
This
study
investigates
expression
pattern,
prognostic
characteristics,
potential
biological
functions
PSMA5
was
significantly
overexpressed
28
types
cancer
when
compared
to
normal
tissue.
Furthermore,
elevated
levels
were
observed
patients
wild-type
isocitrate
dehydrogenase
1
exhibited
positive
correlation
grade.
It
also
found
be
standalone
predictor
outcomes
glioma
patients.Additionally,
inhibiting
PSMA5-induced
cell
cycle
arrest
may
provide
therapeutic
option
for
Frontiers in Immunology,
Год журнала:
2024,
Номер
15
Опубликована: Окт. 9, 2024
Background
As
one
of
the
malignant
tumors
with
highest
incidence
and
fatality
in
world,
colon
adenocarcinoma
(COAD)
has
a
very
complex
pathogenic
mechanism,
which
not
yet
been
fully
elucidated.
Ubiquitin
can
regulate
cell
proliferation,
cycle,
apoptosis,
DNA
damage
repair,
other
processes
by
changing
activity
substrate
proteins
or
causing
ubiquitin-proteasome
degradation.
These
are
key
links
pathogenesis
COAD,
ubiquitin
plays
an
important
role
occurrence
development
COAD.
Methods
We
integrated
transcriptomics,
single-cell
clinical
omics,
TCGA
GEO
databases
COAD
patient
data.
Cox
Lasso
regression
was
employed
to
assess
ubiquitination
genes
for
generating
ubiquitination-related
features.
The
aim
evaluate
prognostic
value
these
features
their
impact
on
immune
microenvironment.
At
same
time,
expression
level
model
further
analyzed
using
Finally,
function
ASNS,
gene
this
trait,
were
detected
vitro
.
Results
In
our
study,
based
identifiable
changes
marker
genes,
feature
be
used
classify
patients
Kaplan-Meier
survival
analysis
indicated
that
those
elevated
risk
scores
each
cohort
experienced
inferior
outcomes.
There
is
good
validation
both
training
queue
queue.
results
infiltration
showed
rate
significantly
increased
high-risk
group.
After
knockdown
signature,
migration
capacity
SW620
RKO
lines
colony
formation
dramatically
reduced
tests.
Conclusion
screened
constructed
features,
as
reliable
indicators
ASNS
identified
possible
biomarker
