PeerJ,
Год журнала:
2024,
Номер
12, С. e18708 - e18708
Опубликована: Дек. 19, 2024
Ferroptosis
is
a
novel
form
of
programmed
cell
death
characterized
by
iron
accumulation,
lipid
peroxidation,
and
decline
in
antioxidant
capacity,
all
which
are
regulated
gene
expression.
The
onset
numerous
diseases
closely
associated
with
ferroptosis.
Common
affect
large
population,
reduce
the
quality
life,
impose
an
increased
burden
on
healthcare
system.
role
ferroptosis
common
diseases,
its
therapeutic
potential,
even
translation
into
clinical
drug
treatments
currently
significant
research
topics
worldwide.
This
study
preliminarily
explores
theoretical
basis
ferroptosis,
mechanism
treatment
prospect
including
ischaemia-reperfusion
injury,
inflammatory
bowel
liver
fibrosis,
acute
kidney
diabetic
disease,
stroke,
Alzheimer’s
cardiovascular
immune
cancer.
review
provides
foundation
for
further
development
as
well
prevention
diseases.
Medicine,
Год журнала:
2025,
Номер
104(3), С. e41218 - e41218
Опубликована: Янв. 17, 2025
Parkinson
disease
(PD)
is
the
second
most
common
neurodegenerative
disease,
and
its
incidence
climbing
every
year,
but
there
still
a
lack
of
effective
clinical
treatments.
In
recent
years,
many
studies
have
shown
that
ferroptosis
plays
key
role
in
progression
PD.
Most
importantly,
cellular
animal
trials
episodes
PD
can
be
alleviated
by
inhibiting
process,
such
as
utilizing
inhibitors,
chelating
agents,
others.
Here,
we
review
ferroptosis,
new
form
cell
death,
pathogenesis
PD,
summarize
therapeutic
strategies
for
targeting
hoping
to
provide
thinking
study
development
strategies.
Journal of Clinical and Translational Hepatology,
Год журнала:
2025,
Номер
000(000), С. 000 - 000
Опубликована: Янв. 22, 2025
Solute
carrier
(SLC)
family
transporters
are
crucial
transmembrane
proteins
responsible
for
transporting
various
molecules,
including
amino
acids,
electrolytes,
fatty
and
nucleotides.
To
date,
more
than
fifty
SLC
transporter
subfamilies
have
been
identified,
many
of
which
linked
to
the
progression
hepatic
steatosis
fibrosis.
These
conditions
often
caused
by
factors
such
as
non-alcoholic
liver
disease
steatohepatitis,
major
contributors
global
burden.
The
activity
members
regulates
transport
substrates
across
biological
membranes,
playing
key
roles
in
lipid
synthesis
metabolism,
mitochondrial
function,
ferroptosis.
processes,
turn,
influence
function
hepatocytes,
stellate
cells,
macrophages,
thereby
contributing
development
Additionally,
some
involved
drug
transport,
acting
critical
regulators
drug-induced
steatosis.
Beyond
substrate
certain
also
exhibit
additional
functions.
Given
pivotal
role
fibrosis,
this
review
aimed
summarize
molecular
mechanisms
through
these
conditions.
International Journal of Molecular Sciences,
Год журнала:
2025,
Номер
26(3), С. 1075 - 1075
Опубликована: Янв. 26, 2025
Major
depressive
disorder
(MDD)
is
a
widespread
and
severe
mental
health
condition
characterized
by
persistent
low
mood
loss
of
interest.
Emerging
evidence
suggests
that
ferroptosis,
an
iron-dependent
form
cell
death,
epigenetic
dysregulation
contribute
to
the
pathogenesis
MDD.
This
study
investigates
role
RNA
demethylase
FTO
autophagy
regulator
BECN1
in
ferroptosis
their
regulation
active
compound
ginsenoside
Rb1
(GRb1)
as
potential
antidepressant
strategy.
Hippocampal
tissues
from
postmortem
MDD
patient
brains
mice
with
chronic
restraint
stress
(CRS)-induced
depression
were
analyzed.
Ferroptosis
was
evaluated
analyzing
levels
markers
such
glutathione
(GSH)
malondialdehyde
(MDA).
GRb1
administered
CRS
model
gavage
explore
its
effects
on
ferroptosis-related
pathways.
The
results
showed
expression
reduced
hippocampal
patients
mice,
promoting
via
disruption
antioxidant
system.
Moreover,
treatment
increased
expression,
modulated
m6A
methylation,
restored
balance,
inhibited
mice.
These
findings
reveal
novel
mechanism
highlight
promising
agent
for
treating
through
targeting
Arsenic
is
a
prevalent
environmental
pollutant
with
recognized
carcinogenic
properties.
Liver
fibrosis
frequent
consequence
of
arsenic
poisoning,
the
activation
hepatic
stellate
cells
(HSCs)
being
central
event.
Solute
Carrier
Family
7
Member
11
(SLC7A11),
pivotal
regulator
ferroptosis,
may
be
involved
in
process
arsenic-induced
liver
fibrosis.
This
study
utilized
lentiviral
vector-mediated
SLC7A11
silencing
LX-2
(a
type
human
cells)
to
establish
an
knockout
cell
model,
which
was
then
exposed
sodium
arsenite
(NaAsO2).
Protein
interactions
were
assessed
through
Immunoprecipitation
(IP),
and
protein
levels
evaluated
via
Western
blot
analysis.
It
found
that
NaAsO2
decreased
cellular
Fe2+
nuclear
receptor
co-activator
4
(NCOA4)
expression,
reversing
these
effects.
Additionally,
IP
analysis
revealed
interaction
between
Beclin1
proteins
NaAsO2.
Silencing
attenuated
reduction
Tumor
p53(P53),
p-mammalian
target
rapamycin
(p-mTOR)
levels,
along
rise
Beclin1,
Phosphorylated
adenosine
monophosphate
activated
kinase
(p-AMPK),
α-smooth
muscle
actin
(α-SMA)
Fibroblast
protein-α
(FAP)
induced
by
Consequently,
promoted
reduced
autophagy
P53/AMPK/mTOR
pathway,
inhibited
HSC
NaAsO2,
potentially
mitigating
Engineered Regeneration,
Год журнала:
2024,
Номер
5(3), С. 283 - 294
Опубликована: Июнь 21, 2024
Non-alcoholic
fatty
liver
disease
(NAFLD),
a
type
of
for
which
no
treatment
is
currently
approved,
remains
major
concern
worldwide.
It
manifested
as
simple
hepatocyte
steatosis
and
can
develop
into
inflammation,
fibrosis,
cirrhosis
cancer
in
severe
cases.
However,
due
to
the
lack
appropriate
vitro
drug
testing
platforms,
an
in-depth
understanding
therapeutic
activity
ginsenoside
Rb1
NAFLD
challenging.
Here,
we
proposed
model
on
organoids
(LOs)-on-a-chip
platform
evaluate
effect
dynamic,
multi-condition
high-throughput
manner.
This
allowed
us
reshape
certain
features
such
multicellular
types
liver-specific
functions
physiology
human-relative
liver.
Free
acids
(FFAs)-induced
LOs
displayed
typical
pathological
characteristics
progression,
including
steatosis,
oxidative
stress,
lipid
peroxidation,
inflammation
fibrosis.
With
intervention,
these
be
significantly
improved,
may
provide
new
insights
potential
mechanisms
progression
suggest
clinical
implications
humans.
The
system
enables
formation,
differentiation,
function
serve
scalable,
sensitive
model,
potentially
expedite
discovery.
