International Immunopharmacology,
Год журнала:
2024,
Номер
143, С. 113492 - 113492
Опубликована: Окт. 30, 2024
Sepsis-induced
acute
liver
injury
(SALI),
a
manifestation
of
sepsis
multi-organ
dysfunction
syndrome,
is
associated
with
poor
prognosis
and
high
mortality.
The
diversity
plasticity
macrophage
subpopulations
explain
their
different
functional
responses
in
diseases.
Kupffer
macrophages,
capsular
monocyte-derived
macrophages
are
involved
pathogen
recognition
clearance
the
regulation
inflammatory
responses,
exacerbating
progression
SALI
through
pathways
pyroptosis,
ferroptosis,
autophagy.
Concurrently,
they
play
an
important
role
maintaining
hepatic
homeostasis
repair
processes
SALI.
Other
recruited
to
diseased
tissues
under
pathological
conditions
polarized
into
various
phenotypes
(mainly
M1
M2
types)
influence
signaling
molecules,
transcription
factors,
metabolic
reprogramming,
thereby
exerting
roles
functions.
This
review
provides
overview
immune
discusses
multiple
provide
reference
for
future
studies.
Molecular Biomedicine,
Год журнала:
2023,
Номер
4(1)
Опубликована: Окт. 16, 2023
Abstract
Ferroptosis,
a
regulated
form
of
cellular
death
characterized
by
the
iron-mediated
accumulation
lipid
peroxides,
provides
novel
avenue
for
delving
into
intersection
metabolism,
oxidative
stress,
and
disease
pathology.
We
have
witnessed
mounting
fascination
with
ferroptosis,
attributed
to
its
pivotal
roles
across
diverse
physiological
pathological
conditions
including
developmental
processes,
metabolic
dynamics,
oncogenic
pathways,
neurodegenerative
cascades,
traumatic
tissue
injuries.
By
unraveling
intricate
underpinnings
molecular
machinery,
contributors,
signaling
conduits,
regulatory
networks
governing
researchers
aim
bridge
gap
between
intricacies
this
unique
mode
multifaceted
implications
health
disease.
In
light
rapidly
advancing
landscape
ferroptosis
research,
we
present
comprehensive
review
aiming
at
extensive
in
origins
progress
human
diseases.
This
concludes
careful
analysis
potential
treatment
approaches
carefully
designed
either
inhibit
or
promote
ferroptosis.
Additionally,
succinctly
summarized
therapeutic
targets
compounds
that
hold
promise
targeting
within
various
facet
underscores
burgeoning
possibilities
manipulating
as
strategy.
summary,
enriched
insights
both
investigators
practitioners,
while
fostering
an
elevated
comprehension
latent
translational
utilities.
revealing
basic
processes
investigating
possibilities,
crucial
resource
scientists
medical
aiding
deep
understanding
effects
situations.
Biomedicine & Pharmacotherapy,
Год журнала:
2024,
Номер
174, С. 116512 - 116512
Опубликована: Апрель 3, 2024
GPX4
(Glutathione
peroxidase
4)
serves
as
a
crucial
intracellular
regulatory
factor,
participating
in
various
physiological
processes
and
playing
significant
role
maintaining
the
redox
homeostasis
within
body.
Ferroptosis,
form
of
iron-dependent
non-apoptotic
cell
death,
has
gained
considerable
attention
recent
years
due
to
its
involvement
multiple
pathological
processes.
is
closely
associated
with
ferroptosis
functions
primary
inhibitor
this
process.
Together,
contribute
pathophysiology
several
diseases,
including
sepsis,
nervous
system
ischemia
reperfusion
injury,
cardiovascular
cancer.
This
review
comprehensively
explores
roles
impacts
development
progression
these
aim
providing
insights
for
identifying
potential
therapeutic
strategies
future.
Cell Death Discovery,
Год журнала:
2023,
Номер
9(1)
Опубликована: Дек. 18, 2023
Ferritinophagy,
a
process
involving
selective
autophagy
of
ferritin
facilitated
by
nuclear
receptor
coactivator
4
(NCOA4),
entails
the
recognition
NCOA4
and
subsequent
delivery
to
autophagosome.
Within
autophagosome,
undergoes
degradation,
leading
release
iron
in
lysosome.
It
is
worth
noting
that
excessive
levels
can
trigger
cell
death.
Recent
evidence
has
elucidated
significant
roles
played
ferritinophagy
ferroptosis
regulation
initiation
progression
cancer.
Given
crucial
role
tumor
biology,
it
may
serve
as
potential
target
for
future
anti-tumor
therapeutic
interventions.
In
this
study,
we
have
provided
distinctive
features
its
distinctions
from
ferroptosis.
Moreover,
briefly
examined
fundamental
regulatory
mechanisms
ferritinophagy,
encompassing
involvement
specific
NCOA4,
Nrf2/HO-1
signaling
other
pathways.
Subsequently,
synthesized
current
understanding
impact
on
cancer
applications,
with
particular
emphasis
utilization
chemotherapy,
nanomaterials,
immunotherapy
pathway
purposes.
Neurochemical Research,
Год журнала:
2024,
Номер
49(8), С. 1965 - 1979
Опубликована: Июнь 4, 2024
Abstract
Cerebral
ischemia–reperfusion
injury
(CIRI)
is
the
second
leading
cause
of
death
worldwide,
posing
a
huge
risk
to
human
life
and
health.
Therefore,
investigating
pathogenesis
underlying
CIRI
developing
effective
treatments
are
essential.
Ferroptosis
an
iron-dependent
mode
cell
death,
which
caused
by
disorders
in
iron
metabolism
lipid
peroxidation.
Previous
studies
demonstrated
that
ferroptosis
also
form
autophagic
nuclear
receptor
coactivator
4(NCOA4)
mediated
ferritinophagy
was
found
regulate
interfering
with
metabolism.
Ferritinophagy
important
pathogenic
mechanisms
CIRI.
This
review
mainly
summarizes
link
regulation
between
further
discusses
their
In
addition,
potential
treatment
methods
targeting
for
presented,
providing
new
ideas
prevention
clinical
future.
Lung
ischemia–reperfusion
(I/R)
injury
is
a
common
clinical
pathology
associated
with
high
mortality.
The
pathophysiology
of
lung
I/R
involves
ferroptosis
and
elevated
protein
O-GlcNAcylation
levels,
while
the
effect
on
remains
unclear.
This
research
aimed
to
explore
reducing
in
pulmonary
epithelial
cells
caused
by
I/R.
First,
we
identified
O-GlcNAc
transferase
1
(Ogt1)
as
differentially
expressed
gene
acute
injury/acute
respiratory
distress
syndrome
(ALI/ARDS)
patients,
using
single-cell
sequencing,
Gene
Ontology
analysis
(GO
analysis)
revealed
enrichment
process.
We
found
time-dependent
dynamic
alteration
during
injury.
Proteomics
proteins
enriched
multiple
redox-related
pathways
based
KEGG
annotation.
Thus,
generated
Ogt1-conditional
knockout
mice
that
Ogt1
deficiency
aggravated
ferroptosis,
evidenced
lipid
reactive
oxygen
species
(lipid
ROS),
malondialdehyde
(MDA),
Fe2+,
well
alterations
critical
expression
glutathione
peroxidase
4
(GPX4)
solute
carrier
family
7
member
11
(SLC7A11).
Consistently,
inhibited
sensitivity
hypoxia/reoxygenation
(H/R)
injury-induced
TC-1
via
O-GlcNAcylated
NF-E2-related
factor-2
(Nrf2).
Furthermore,
both
chromatin
immunoprecipitation
(ChIP)
assay
dual-luciferase
reporter
indicated
Nrf2
could
bind
translation
start
site
(TSS)
glucose-6-phosphate
dehydrogenase
(G6PDH)
promote
its
transcriptional
activity.
As
an
important
rate-limiting
enzyme
pentose
phosphate
pathway
(PPP),
G6PDH
provided
mass
nicotinamide
adenine
dinucleotide
(NADPH)
improve
redox
state
(GSH)
eventually
led
resistance.
Rescue
experiments
proved
knockdown
or
Nrf2-T334A
(O-GlcNAcylation
site)
mutation
abolished
protective
In
summary,
protect
against
Nrf2/G6PDH
pathway.
Our
work
will
provide
new
basis
for
therapeutic
strategies
ischemia–reperfusion-induced
Food & Function,
Год журнала:
2023,
Номер
14(16), С. 7692 - 7704
Опубликована: Янв. 1, 2023
Nobiletin
(NOB),
a
plant-based
polymethoxyflavone,
is
promising
protective
agent
against
sepsis;
yet
the
mechanisms
were
not
fully
elucidated.
The
gut
microbiota
found
to
be
strongly
associated
with
sepsis-associated
acute
liver
injury
(SALI).
Here,
our
study
aimed
evaluate
effect
of
NOB
on
SALI
and
explore
underlying
molecular
mechanisms.
Cecal
ligation
puncture
(CLP)
was
used
induce
in
mice.
administered
by
gavage
for
7
days
before
CLP
induction.
16S
rRNA
gene
sequencing
fecal
transplantation
(FMT)
performed
verify
function
microbiota.
markers
ferroptosis,
inflammation,
composition,
determined.
administration
significantly
alleviated
hepatic
ferroptosis
inflammation
septic
Meanwhile,
upregulated
expression
levels
nuclear
factor
E2-related
2
(Nrf2)
its
downstream
protein
heme
oxygenase-1
(HO-1).
mice
reversed
Nrf2
inhibitor
ML385.
Additionally,
increased
abundances
Ligilactobacillus,
Akkermansia,
Lactobacillus,
decreased
Dubosiella
Bacteroides
observed
under
administration,
suggesting
that
might
modulate
composition
Furthermore,
ablation
antibiotic
treatment
partly
effects
sepsis.
FMT
also
confirmed
inhibited
activated
signalling
modulating
These
results
revealed
that,
microbiota,
attenuated
through
upregulating
Nrf2-Gpx4.
Our
findings
provide
novel
insights
into
microbiome-based
therapeutic
approaches
