Journal of Zhejiang University (Medical Sciences),
Год журнала:
2024,
Номер
53(6), С. 747 - 755
Опубликована: Дек. 1, 2024
As
the
central
organ
of
metabolism,
liver
plays
a
pivotal
role
in
regulation
synthesis
and
metabolism
various
nutrients
within
body.
Ferroptosis,
as
newly
discovered
type
programmed
cell
death
caused
by
accumulation
iron-dependent
lipid
peroxides,
is
involved
physiological
pathological
processes
variety
acute
chronic
diseases.
Ferroptosis
can
accelerate
pathogenetic
process
injury,
metabolic
associated
fatty
disease,
alcoholic
viral
hepatitis,
autoimmune
hepatitis;
while
it
slower
disease
progression
advanced
fibrosis
hepatocellular
carcinoma.
This
suggests
that
targeted
ferroptosis
may
impact
occurrence
development
article
reviews
latest
research
progress
diseases,
including
It
aims
to
provide
insights
for
prevention
treatment
diseases
through
targeting
ferroptosis.
Ferroptosis
is
a
nonapoptotic
form
of
cell
death
characterized
by
iron-dependent
lipid
peroxidation
in
membrane
phospholipids.
Since
its
identification
2012,
extensive
research
has
unveiled
involvement
the
pathophysiology
numerous
diseases,
including
cancers,
neurodegenerative
disorders,
organ
injuries,
infectious
autoimmune
conditions,
metabolic
and
skin
diseases.
Oxidizable
lipids,
overload
iron,
compromised
antioxidant
systems
are
known
as
critical
prerequisites
for
driving
overwhelming
peroxidation,
ultimately
leading
to
plasma
rupture
ferroptotic
death.
However,
precise
regulatory
networks
governing
ferroptosis
ferroptosis-targeted
therapy
these
diseases
remain
largely
undefined,
hindering
development
pharmacological
agonists
antagonists.
In
this
review,
we
first
elucidate
core
mechanisms
summarize
epigenetic
modifications
(e.g.,
histone
modifications,
DNA
methylation,
noncoding
RNAs,
N6-methyladenosine
modification)
nonepigenetic
genetic
mutations,
transcriptional
regulation,
posttranslational
modifications).
We
then
discuss
association
between
disease
pathogenesis
explore
therapeutic
approaches
targeting
ferroptosis.
also
introduce
potential
clinical
monitoring
strategies
Finally,
put
forward
several
unresolved
issues
which
progress
needed
better
understand
hope
review
will
offer
promise
application
therapies
context
human
health
disease.
Macrophages
play
crucial
roles
in
immune
response
and
tissue
homeostasis,
with
their
functions
becoming
increasingly
complex
obesity-mediated
metabolic
disorders.
This
review
explores
the
extensive
range
of
macrophage
activities
within
adipose
liver
tissues,
emphasizing
contribution
to
pathogenesis
progression
obesity
its
related
dysfunction-associated
steatotic
disease
(MASLD).
In
context
obesity,
macrophages
respond
adaptively
lipid
overloads
inflammatory
cues
tissue,
profoundly
influencing
insulin
resistance
homeostasis.
Concurrently,
role
extends
moderating
inflammation
orchestrating
fibrotic
responses,
integral
development
MASLD.
Highlighting
spectrum
phenotypes
across
these
landscapes,
we
summarize
diverse
linking
processes
functions.
advocates
for
a
deeper
understanding
subsets
proposing
targeted
research
harness
therapeutic
potential
mitigating
MASLD
other
Biomedicines,
Год журнала:
2025,
Номер
13(3), С. 683 - 683
Опубликована: Март 10, 2025
Iron
overload
can
lead
to
increased
deposition
of
iron
and
cause
organ
damage
in
the
liver,
pancreas,
heart
synovium.
disorders
are
due
either
genetic
or
acquired
abnormalities
such
as
excess
transfusions
chronic
liver
diseases.
The
most
common
disease
is
classic
hemochromatosis
(HH)
type
1,
which
caused
by
mutations
HFE.
Other
rare
forms
HH
include
2A
with
at
gene
hemojuvelin
2B
HAMP
that
encodes
hepcidin.
3,
transferrin
receptor
2.
Mutations
SLC40A1
ferroportin
4A
4B.
In
present
review,
an
overview
metabolism
including
absorption
enterocytes
regulation
macrophages,
sinusoidal
endothelial
cells
(LSECs)
hepatocyte
production
hepcidin
presented.
Hereditary
Hemochromatosis
current
pathogenetic
model
analyzed.
Finally,
a
new
hypothesis
based
on
published
data
was
suggested.
Kupffer
cell
primary
defect
HFE
(and
possibly
types
2
3),
while
hepcidin-relative
deficiency,
underlying
abnormality
three
HH,
secondary
consequence.
Toxics,
Год журнала:
2025,
Номер
13(4), С. 265 - 265
Опубликована: Март 31, 2025
Nickel
oxide
nanoparticles
(NiONPs)
can
induce
liver
fibrosis,
and
their
mechanism
may
be
related
to
non-coding
RNA,
nuclear
receptor
signal
transduction
ferroptosis,
but
the
regulatory
relationship
between
them
is
not
clear.
In
this
study,
we
aimed
investigate
role
of
hsa_circ_0001944
in
regulating
Farnesol
X
(FXR)/Toll-like
4
(TLR4)
pathway
ferroptosis
NiONPs-induced
collagen
deposition.
We
observed
decreased
FXR
expression,
increased
TLR4
expression
alterations
features
both
rat
fibrosis
LX-2
cell
deposition
model.
To
among
FXR,
treated
cells
with
agonist
(GW4064),
inhibitor
(TAK-242)
(Erastin)
combined
NiONPs.
The
results
showed
that
TAK-242
alleviated
by
increasing
features.
Furthermore,
GW4064
reduced
TLR4,
indicated
inhibited
enhanced
features,
which
were
involved
process
induced
Subsequently,
predicted
might
regulate
through
bioinformatics
analysis,
found
NiONPs
cells.
Overexpression
level,
summary,
demonstrated
regulates
FXR/TLR4
alleviate
formation
European journal of medical research,
Год журнала:
2025,
Номер
30(1)
Опубликована: Апрель 11, 2025
This
study
aimed
to
explore
the
causal
association
between
imaging
measurement
indicators
of
major
internal
organs
and
liver
lesions
using
a
two-sample
Mendelian
randomization
(MR)
method.
Data
from
UK
Biobank
GWAS
Catalog
platform
were
used
select
single
nucleotide
polymorphisms
(SNPs)
associated
with
MRI
or
derived
results
various
organ
as
genetic
instrumental
variables.
FinnGen
project's
R9
version
lesion
outcomes,
such
nonalcoholic
fatty
disease
(NAFLD),
cirrhosis,
primary
hepatocellular
carcinoma
(HCC).
UVMR
analysis
utilized
variable-by-variable,
MVMR
was
adjust
for
confounding
on
significant
Steiger
directional
test,
heterogeneity,
pleiotropy,
sensitivity
tests
conducted
enhance
reliability.
Univariate
(UVMR)
indicated
that
volume
(LV),
fat
(LF),
subcutaneous
adipose
tissue
(SATM)
are
risk
factors
NAFLD.
The
multivariable
MR
(MVMR)
NAFLD
showed
LV
LF
remained
significant,
while
SATM
did
not.
For
cirrhosis
(NAC),
suggested
LV,
LF,
factors,
but
only
significant.
Additionally,
pancreatic
(PV)
found
be
protective
factor,
splenic
(SV)
pathogenic
factor
NAC.
HCC,
both
analyses
iron
(LI)
not
remain
in
analysis.
In
NAC
stage,
additional
effects
PV
SV
observed.
related
LI
support
effect
HCC
stage.
