Ferroptosis inhibitors: past, present and future
Frontiers in Pharmacology,
Год журнала:
2024,
Номер
15
Опубликована: Май 23, 2024
Ferroptosis
is
a
non-apoptotic
mode
of
programmed
cell
death
characterized
by
iron
dependence
and
lipid
peroxidation.
Since
the
ferroptosis
was
proposed,
researchers
have
revealed
mechanisms
its
formation
continue
to
explore
effective
inhibitors
in
disease.
Recent
studies
shown
correlation
between
pathological
neurodegenerative
diseases,
as
well
diseases
involving
tissue
or
organ
damage.
Acting
on
ferroptosis-related
targets
may
provide
new
strategies
for
treatment
ferroptosis-mediated
diseases.
This
article
specifically
describes
metabolic
pathways
summarizes
reported
action
natural
synthetic
small
molecule
their
efficacy
The
paper
also
treatments
such
gene
therapy,
nanotechnology,
summarises
challenges
encountered
clinical
translation
inhibitors.
Finally,
relationship
other
modes
discussed,
hopefully
paving
way
future
drug
design
discovery.
Язык: Английский
Rosmarinic acid Liposomes Suppress Ferroptosis in Ischemic Brain via Inhibition of TfR1 in BMECs
Phytomedicine,
Год журнала:
2024,
Номер
132, С. 155835 - 155835
Опубликована: Июнь 28, 2024
Язык: Английский
A new strategy for the treatment of intracerebral hemorrhage: Ferroptosis
Experimental Neurology,
Год журнала:
2024,
Номер
382, С. 114961 - 114961
Опубликована: Сен. 15, 2024
Язык: Английский
Inhibition of Phosphodiesterase 4 Suppresses Neuronal Ferroptosis After Cerebral Ischemia/Reperfusion
Molecular Neurobiology,
Год журнала:
2024,
Номер
unknown
Опубликована: Сен. 17, 2024
Язык: Английский
Post-cerebral ischemia energy crisis: the role of glucose metabolism in the energetic crisis
Brain Injury,
Год журнала:
2025,
Номер
unknown, С. 1 - 11
Опубликована: Апрель 16, 2025
Cells
universally
employ
an
efficiency-driven
metabolic
switch
mechanism
during
nutritional
changes,
growth,
and
differentiation,
transitioning
from
oxidative
phosphorylation
(OXPHOS)
to
glycolysis
ensure
survival
under
hypoxic
conditions
or
high
energy
demands.
In
cerebral
ischemia,
inadequate
blood
supply
causes
oxygen
deprivation,
prompting
brain
cells
initiate
glycolytic
reprogramming
meet
urgent
needs.
While
this
adaptation
is
a
temporary
solution,
it
may
lead
lactic
acidosis,
aggravated
inflammation,
increased
free
radical
production.
Prolonged
reperfusion
with
sustained
can
exacerbate
cell
damage,
potentially
causing
irreversible
harm.
This
review
systematically
examines
the
dynamic
changes
in
glucose
transport
mechanisms
roles
of
immediate,
early,
intermediate,
late
responder
cells,
along
their
regulatory
factors,
reprogramming.
Using
temporal
analysis
framework
based
on
body's
natural
response
sequence
pathological
events,
we
elucidate
how
at
different
stages
collaborate
address
metabolism
conditions.
Reversing
inhibiting
improve
processes
ischemic
stroke,
offering
potential
therapeutic
benefits.
Язык: Английский
Electroacupuncture Inhibits Ferroptosis by Modulating Iron Metabolism and Oxidative Stress to Alleviate Cerebral Ischemia–Reperfusion Injury
Journal of Molecular Neuroscience,
Год журнала:
2025,
Номер
75(2)
Опубликована: Май 3, 2025
Ischemic
stroke
(IS)
is
one
of
the
leading
causes
mortality
and
long-term
disability
worldwide.
Electroacupuncture
(EA)
commonly
used
in
treatment
IS,
meaning
that
may
reduce
cerebral
ischemia-reperfusion
injury
(CIRI).
The
middle
artery
occlusion/reperfusion
(MCAO/R)
rat
models
were
created
by
modified
Zea
Longa
suture
method.
EA
was
performed
for
7
consecutive
days
at
acupoints
Neiguan
(PC6),
Shuigou
(GV26),
Sanyinjiao
(SP6).
neurological
function
assessed
using
Zausinger
six-point
deficiency
score.
infarct
volume
detected
2,3,5-triphenyl
tetrazolium
chloride
(TTC)
staining.
Hematoxylin
eosin
(HE)
staining
employed
to
observe
pathological
changes
brain
tissues.
Prussian
blue
investigate
iron
deposition
within
Transmission
electron
microscopy
(TEM)
utilized
examine
morphological
characteristics
mitochondria.
Simultaneously,
flow
cytometry
detect
fluorescence
intensity
reactive
oxygen
species
(ROS).
Assay
kits
measure
levels
Fe2+
glutathione
(GSH).
Additionally,
western
blot
(WB)
real-time
quantitative
polymerase
chain
reaction
(RT-qPCR)
assays
evaluate
expression
proteins
associated
with
ferroptosis.
Compared
MCAO/R
group,
both
+
DFO
groups
exhibited
significant
improvements
following
(CIR),
attenuated
tissue
injury,
reduced
tissue.
Furthermore,
displayed
a
marked
reduction
mitochondrial
injury.
There
substantial
decrease
ROS
levels,
accompanied
notable
increase
GSH
level
peroxidase
4
(GPX4)
activity.
ferroportin1
(FPN1)
protein
mRNA
significantly
increased
groups,
transferrin
(TF),
receptor
1
(TFR1),
divalent
metal
transporter
(DMT1)
mRNA,
as
well
ferritin
(FER)
protein,
decreased.
inhibits
ferroptosis
modulating
metabolism
oxidative
stress
alleviate
CIRI,
exerting
neuroprotective
effects.
Язык: Английский
Mechanistic role of environmental toxicants in inducing cellular ferroptosis and its associated diseases
Ecotoxicology and Environmental Safety,
Год журнала:
2025,
Номер
298, С. 118269 - 118269
Опубликована: Май 10, 2025
Язык: Английский
Molecular Changes in the Ischemic Brain as Non-Invasive Brain Stimulation Targets—TMS and tDCS Mechanisms, Therapeutic Challenges, and Combination Therapies
Biomedicines,
Год журнала:
2024,
Номер
12(7), С. 1560 - 1560
Опубликована: Июль 13, 2024
Ischemic
stroke
is
one
of
the
leading
causes
death
and
disability.
As
currently
used
neurorehabilitation
methods
present
several
limitations,
ongoing
research
focuses
on
use
non-invasive
brain
stimulation
(NIBS)
techniques
such
as
transcranial
magnetic
(TMS)
direct
current
(tDCS).
NIBS
were
demonstrated
to
modulate
neural
excitability
improve
motor
cognitive
functioning
in
neurodegenerative
diseases.
However,
their
mechanisms
action
are
not
fully
elucidated,
clinical
outcomes
often
unpredictable.
This
review
explores
molecular
processes
underlying
effects
TMS
tDCS
rehabilitation,
including
oxidative
stress
reduction,
cell
death,
neurogenesis,
neuroprotective
phenotypes
glial
cells.
A
highlight
put
newly
emerging
therapeutic
targets,
ferroptotic
pyroptotic
pathways.
In
addition,
issue
interindividual
variability
discussed,
role
neuroimaging
investigated
get
closer
personalized
medicine.
Furthermore,
translational
challenges
analyzed,
limitations
trials
investigated.
The
paper
concludes
with
suggestions
for
further
treatment,
putting
focus
combination
therapies,
well
novel
protocols
techniques.
Язык: Английский