The FASEB Journal,
Год журнала:
2024,
Номер
38(11)
Опубликована: Май 30, 2024
Abstract
Ischemia–reperfusion
(IR)
injury
is
primarily
characterized
by
the
restoration
of
blood
flow
perfusion
and
oxygen
supply
to
ischemic
tissue
organs,
but
it
paradoxically
leads
aggravation.
IR
a
challenging
pathophysiological
process
that
difficult
avoid
clinically
frequently
occurs
during
organ
transplantation,
surgery,
shock
resuscitation,
other
processes.
The
major
causes
include
increased
levels
free
radicals,
calcium
overload,
oxidative
stress,
excessive
inflammatory
response.
Ghrelin
newly
discovered
brain‐intestinal
peptide
with
anti‐inflammatory
antiapoptotic
effects
improve
supply.
role
mechanism
ghrelin
in
intestinal
ischemia–reperfusion
(IIR)
remain
unclear.
We
hypothesized
could
attenuate
IIR‐induced
stress
apoptosis.
To
investigate
this,
we
established
IIR
using
non‐invasive
arterial
clip
clamp
root
superior
mesenteric
artery
(SMA)
mice.
was
injected
intraperitoneally
at
dose
50
μg/kg
20
min
before
[D‐Lys3]‐GHRP‐6
12
nmol/kg
injection.
mimicked
hypoxia‐reoxygenation
(HR)
Caco‐2
cells,
which
are
similar
epithelial
cells
structure
biochemistry.
Our
results
showed
inhibited
IIR/HR‐induced
apoptosis
activating
GHSR‐1α.
Moreover,
found
activated
GHSR‐1α/Sirt1/FOXO1
signaling
pathway.
further
Sirt1
critical
for
ghrelin‐mediated
mitigation
IIR/HR
injury.
Overall,
our
data
suggest
pretreatment
reduces
binding
GHSR‐1α
activate
Sirt1.
Signal Transduction and Targeted Therapy,
Год журнала:
2024,
Номер
9(1)
Опубликована: Окт. 14, 2024
Iron,
an
essential
mineral
in
the
body,
is
involved
numerous
physiological
processes,
making
maintenance
of
iron
homeostasis
crucial
for
overall
health.
Both
overload
and
deficiency
can
cause
various
disorders
human
diseases.
Ferroptosis,
a
form
cell
death
dependent
on
iron,
characterized
by
extensive
peroxidation
lipids.
Unlike
other
kinds
classical
unprogrammed
death,
ferroptosis
primarily
linked
to
disruptions
metabolism,
lipid
peroxidation,
antioxidant
system
imbalance.
Ferroptosis
regulated
through
transcription,
translation,
post-translational
modifications,
which
affect
cellular
sensitivity
ferroptosis.
Over
past
decade
or
so,
diseases
have
been
as
part
their
etiology,
including
cancers,
metabolic
disorders,
autoimmune
diseases,
central
nervous
cardiovascular
musculoskeletal
Ferroptosis-related
proteins
become
attractive
targets
many
major
that
are
currently
incurable,
some
regulators
shown
therapeutic
effects
clinical
trials
although
further
validation
potential
needed.
Therefore,
in-depth
analysis
its
molecular
mechanisms
may
offer
additional
strategies
prevention
treatment.
In
this
review,
we
discuss
significance
contribution
etiology
development
along
with
evidence
supporting
targeting
approach.
Importantly,
evaluate
recent
promising
interventions,
providing
guidance
future
targeted
treatment
therapies
against
International Journal of Biological Sciences,
Год журнала:
2024,
Номер
20(13), С. 5145 - 5161
Опубликована: Янв. 1, 2024
Non-small
cell
lung
cancer
(NSCLC),
a
major
subtype
of
cancer,
encompasses
squamous
carcinoma,
adenocarcinoma,
and
large
carcinoma.
Compared
to
small
NSCLC
cells
grow
divide
more
slowly,
their
metastasis
occurs
at
later
stage.
Currently,
chemotherapy
is
the
primary
treatment
for
this
disease.
Sappanone
A
(SA)
flavonoid
compound
extracted
from
plant
Caesalpinia
sappan,
known
its
antitumor,
redox-regulating,
anti-inflammatory
properties.
Recent
studies
have
investigated
interaction
SA
with
mitochondrial
pathways
in
regulating
death
through
Nrf-2/GPX-4/xCT
axis.
This
study
specifically
explores
mechanism
by
which
affects
morphology
structure
regulation
mitophagy
biogenesis
tumor
cells.
The
primarily
utilizes
second-generation
transcriptomic
sequencing
data
molecular
docking
techniques
elucidate
role
programmed
omics
results
indicate
that
significantly
targets
genes
involved
oxidative
phosphorylation,
mitophagy,
dynamics,
stress.
Further
findings
confirmed
Nrf-2/GPX4/xCT
pathway
serves
as
crucial
target
NSCLC.
Knockdown
Nrf-2
(si-Nrf-2)
overexpression
(ad-Nrf-2)
were
shown
modulate
therapeutic
efficacy
varying
degrees.
Additionally,
modifications
GPX4/xCT
affected
regulatory
effects
on
autophagy,
biogenesis,
energy
metabolism.
These
mechanisms
may
be
mediated
caspase
ferroptosis-related
signaling.
Molecular
biology
experiments
demonstrated
intervention
further
inhibits
phosphorylation
FUNDC1
Tyr18
downregulates
TOM20
expression.
was
found
reduce
expression
PGC1α,
Nrf-1,
Tfam,
resulting
decrease
respiration
Overexpression
counteract
biogenesis.
Confocal
microscopy
revealed
increases
fragmentation,
subsequently
inducing
pathway-mediated
death.
However,
genetic
modification
altered
In
conclusion,
has
been
identified
promising
agent
apoptosis
ferroptosis
represent
key
Targeting
axis
offers
novel
approach
maintaining
homeostasis
within
cellular
microenvironment.
Cell Death and Disease,
Год журнала:
2024,
Номер
15(11)
Опубликована: Ноя. 26, 2024
Abstract
Regulated
cell
death
(RCD)
refers
to
the
form
of
that
can
be
regulated
by
various
biomacromolecules.
Each
modalities
have
their
distinct
morphological
changes
and
molecular
mechanisms.
However,
intense
evidences
suggest
lipid
peroxidation
common
feature
initiates
propagates
death.
Excessive
alters
property
membrane
further
damage
proteins
nucleic
acids,
which
is
implicated
in
human
pathologies.
Here,
we
firstly
review
classical
chain
process
peroxidation,
clarify
current
understanding
myriad
roles
mechanisms
RCD
types.
We
also
discuss
how
involves
diseases
such
intimate
association
between
peroxidation-driven
leveraged
develop
rational
therapeutic
strategies.
Drug
resistance
is
a
common
challenge
in
clinical
tumor
treatment.
A
reduction
drug
sensitivity
of
cells
often
accompanied
by
an
increase
autophagy
levels,
leading
to
autophagy-related
resistance.
The
effectiveness
combining
chemotherapy
drugs
with
inducers/inhibitors
has
been
widely
confirmed,
but
the
mechanisms
are
still
unclear.
Ferroptosis
and
pyroptosis
can
be
affected
various
types
autophagy.
Therefore,
ferroptosis
have
crosstalk
via
autophagy,
potentially
switch
cell
death
under
certain
conditions.
As
two
forms
inflammatory
programmed
death,
different
effects
on
inflammation,
cGAS-STING
signaling
pathway
also
involved.
it
plays
important
role
progression
some
chronic
diseases.
This
review
discusses
relationship
between
pyroptosis,
attempts
uncover
reasons
behind
evasion
nature
Biomarker Research,
Год журнала:
2025,
Номер
13(1)
Опубликована: Янв. 23, 2025
Neutrophil
extracellular
traps
(NETs)
are
intricate,
web-like
formations
composed
of
DNA,
histones,
and
antimicrobial
proteins,
released
by
neutrophils.
These
structures
participate
in
a
wide
array
physiological
pathological
activities,
including
immune
rheumatic
diseases
damage
to
target
organs.
Recently,
the
connection
between
NETs
cancer
has
garnered
significant
attention.
Within
tumor
microenvironment
metabolism,
exhibit
multifaceted
roles,
such
as
promoting
proliferation
migration
cells,
influencing
redox
balance,
triggering
angiogenesis,
driving
metabolic
reprogramming.
This
review
offers
comprehensive
analysis
link
emphasizing
areas
that
remain
underexplored.
include
interaction
with
mitochondria,
their
effect
on
states
within
tumors,
involvement
reprogramming,
contribution
angiogenesis
tumors.
Such
insights
lay
theoretical
foundation
for
deeper
understanding
role
development.
Moreover,
also
delves
into
potential
therapeutic
strategies
suggests
future
research
directions,
offering
new
perspectives
treatment
other
related
diseases.
Biomedicine & Pharmacotherapy,
Год журнала:
2024,
Номер
175, С. 116722 - 116722
Опубликована: Май 9, 2024
Ulcerative
colitis
(UC)
is
a
complex
immune-mediated
chronic
inflammatory
bowel
disease.
It
mainly
characterized
by
diffuse
inflammation
of
the
colonic
and
rectal
mucosa
with
barrier
function
impairment.
Identifying
new
biomarkers
for
development
more
effective
UC
therapies
remains
pressing
task
current
research.
Ferroptosis
newly
identified
form
regulated
cell
death
iron-dependent
lipid
peroxidation.
As
research
deepens,
ferroptosis
has
been
demonstrated
to
be
involved
in
pathological
processes
numerous
diseases.
A
growing
body
evidence
suggests
that
pathogenesis
associated
ferroptosis,
regulation
provides
opportunities
treatment.
However,
specific
mechanisms
which
participates
remain
fully
thoroughly
investigated.
Therefore,
this
review,
we
focus
on
advances
mechanism
recent
years
describe
potential
role
UC.
In
addition,
explore
underlying
crosslinked
pathway
between
other
such
as
macrophages,
neutrophils,
autophagy,
endoplasmic
reticulum
stress,
gut
microbiota
Finally,
also
summarize
compounds
may
act
inhibitors
future.
Cell Death Discovery,
Год журнала:
2024,
Номер
10(1)
Опубликована: Фев. 19, 2024
Abstract
Mitochondria
produce
adenosine
triphosphate
and
potentially
contribute
to
proinflammatory
responses
cell
death.
Mitophagy,
as
a
conservative
phenomenon,
scavenges
waste
mitochondria
their
components
in
the
cell.
Recent
studies
suggest
that
severe
infections
develop
alongside
mitochondrial
dysfunction
mitophagy
abnormalities.
Restoring
protects
against
excessive
inflammation
multiple
organ
failure
sepsis.
Here,
we
review
normal
process,
its
interaction
with
invading
microorganisms
immune
system,
summarize
mechanism
of
during
infection.
We
highlight
critical
role
preventing
International Journal of Biological Sciences,
Год журнала:
2024,
Номер
20(9), С. 3515 - 3529
Опубликована: Янв. 1, 2024
Impaired
angiogenesis
is
a
major
factor
contributing
to
delayed
wound
healing
in
diabetes.
Dysfunctional
mitochondria
promote
the
formation
of
neutrophil
extracellular
traps
(NETs),
obstructing
during
healing.
Mesenchymal
stem
cell-derived
vesicles
(MSC-EVs)
have
shown
promise
promoting
tissue
repair
and
regeneration
diabetes;
however,
precise
pathways
involved
this
process
remain
unclear.
In
study,
NET-induced
ferroptosis
endothelial
cells
(ECs)
were
assessed
diabetic
samples
from
both
patients
animal
models.
