Nutrients,
Год журнала:
2024,
Номер
16(21), С. 3747 - 3747
Опубликована: Окт. 31, 2024
:
Observational
studies
have
noted
that
patients
with
certain
retinal
degenerative
diseases
exhibit
iron
disturbances
in
the
retina
or
vitreous
compared
to
healthy
controls.
However,
connection
between
serum
status
and
these
remains
unclear.
This
study
aims
explore
potential
causal
relationship
biomarkers
development
of
age-related
macular
degeneration
(AMD),
retinitis
pigmentosa
(RP),
diabetic
retinopathy
(DR).
Frontiers in Immunology,
Год журнала:
2024,
Номер
15
Опубликована: Июнь 27, 2024
Ferroptosis,
a
new
type
of
programmed
cell
death
proposed
in
recent
years,
is
characterized
mainly
by
reactive
oxygen
species
and
iron-mediated
lipid
peroxidation
differs
from
death,
such
as
apoptosis,
necrosis,
autophagy.
Ferroptosis
associated
with
variety
physiological
pathophysiological
processes.
Recent
studies
have
shown
that
ferroptosis
can
aggravate
or
reduce
the
occurrence
development
diseases
targeting
metabolic
pathways
signaling
tumors,
ischemic
organ
damage,
other
degenerative
related
to
peroxidation.
Increasing
evidence
suggests
closely
linked
onset
progression
various
ophthalmic
conditions,
including
corneal
injury,
glaucoma,
age-related
macular
degeneration,
diabetic
retinopathy,
retinal
detachment,
retinoblastoma.
Our
review
current
research
on
reveals
significant
advancements
our
understanding
pathogenesis,
aetiology,
treatment
these
conditions.
Pharmacological Research,
Год журнала:
2025,
Номер
212, С. 107579 - 107579
Опубликована: Янв. 5, 2025
The
incidence
of
metabolic
diseases-hypertension,
diabetes,
obesity,
dysfunction-associated
steatotic
liver
disease
(MASLD),
and
atherosclerosis-is
increasing
annually,
imposing
a
significant
burden
on
both
human
health
the
social
economy.
occurrence
development
these
diseases
are
closely
related
to
disruption
ion
homeostasis,
which
is
crucial
for
maintaining
cellular
functions
equilibrium.
However,
specific
mechanism
homeostasis
in
still
unclear.
This
article
reviews
role
pathogenesis
assesses
its
potential
as
therapeutic
target.
Furthermore,
explores
pharmacological
strategies
that
target
channels
transporters,
including
existing
drugs
emerging
under
development.
Lastly,
discusses
direction
future
strategies,
possibility
gene
therapy
targeting
personalized
using
novel
biomarkers.
In
summary,
provides
new
perspective
approach
treatment
diseases.
Experimental and Clinical Endocrinology & Diabetes,
Год журнала:
2025,
Номер
133(03), С. 120 - 132
Опубликована: Март 1, 2025
Abstract
Diabetic
foot
ulcer
(DFU)
represents
a
severe
complication
of
diabetes,
mainly
caused
by
peripheral
vascular
occlusion
and
infection,
presenting
significant
clinical
challenges
in
treatment
potentially
resulting
gangrene,
amputation,
or
even
fatality.
This
study
aimed
to
investigate
the
involvement
underlying
mechanisms
Meteorin-like
(Metrnl)
pathogenic
process
DFU.
Mice
underwent
diabetes
induction
streptozotocin,
while
human
umbilical
vein
endothelial
cells
(HUVECs)
were
exposed
5.5,
10,
20
40
mM
glucose.
HUVECs
transfected
with
negative
Metrnl
si-nc
si-Metrnl
plasmids
via
Lipofectamine
2000.
The
expression
was
down-regulated
both
patients
murine
model
Elevated
glucose
levels
diminished
through
enhanced
ubiquitination.
suppression
exacerbated
mouse
alleviated
oxidative
stress
ferroptosis
DFU
inhibiting
mitochondrial
damage.
induced
liver
kinase
B1
(LKB1)/AMP-activated
protein
(AMPK)
signaling
model.
LKB1
attenuated
effects
on
data
cumulatively
demonstrate
that
ameliorates
damage
LKB1/AMPK
signaling,
suggesting
targeting
may
emerge
as
potential
preventive
approach
against
other
diabetes.
Diabetic Medicine,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 10, 2025
Abstract
Aim
Diabetic
retinopathy
(DR)
represents
the
main
ocular
complication
of
diabetes.
Targeting
ferroptosis
is
a
promising
treatment
choice
for
various
diabetic
complications.
N6‐methyladenosine
(m6A)
demethylase
alkylation
repair
homolog
protein
5
(ALKBH5)
functions
as
pivotal
regulator
ferroptosis,
and
we
investigated
its
role
molecular
mechanisms
in
DR.
Methods
A
DR
mouse
model
was
developed
by
streptozotocin
(STZ)
intraperitoneal
injection.
High
glucose
(HG)‐induced
human
retinal
pigment
epithelial
cells
(ARPE‐19)
were
used
vitro
.
ALKBH5,
YTH
RNA
binding
1
(YTHDF1)
acyl‐CoA
synthetase
long‐chain
family
member
4
(ACSL4)
expression
levels
examined
RT‐qPCR
Western
blot.
The
biological
ALKBH5
vivo
gain‐of‐function
loss‐of‐function
analyses.
ALKBH5's
downstream
regulatory
detected
bioinformatics
analysis,
pull‐down,
MeRIP‐qPCR
actinomycin
D
assay.
Results
under‐expressed
while
YTHDF1
ACSL4
up‐regulated
tissues
STZ‐induced
mice
HG‐stimulated
ARPE‐19
cells.
Ectopically
expressed
or
knockdown
partially
reversed
increased
,
evidenced
decreased
Fe
2+
malondialdehyde
reactive
oxygen
species
yet
glutathione
level.
mediated
m6A
modification
mRNA
disrupted
stability
YTHDF1‐dependent
manner.
Importantly,
data
demonstrated
that
overexpression
repressed
alleviated
down‐regulating
ACSL4.
Conclusion
These
findings
suggest
may
delay
progression
reducing
through
m6A‐YTHDF1‐ACSL4
axis,
offering
therapeutic
paradigms
Frontiers in Endocrinology,
Год журнала:
2025,
Номер
16
Опубликована: Апрель 25, 2025
Diabetic
cardiomyopathy
(DCM)
is
a
common
and
fatal
cardiac
complication
caused
by
diabetes,
with
its
pathogenesis
involving
various
forms
of
cell
death
mitochondrial
dysfunction,
particularly
ferroptosis
injury.
Recent
studies
have
indicated
that
damage
play
crucial
roles
in
the
onset
progression
DCM,
though
their
precise
regulatory
mechanisms
remain
unclear.
Of
particular
interest
interaction
between
damage,
as
well
synergistic
effects,
which
are
not
fully
understood.
This
review
summarizes
injury
DCM
explores
molecular
involved,
an
emphasis
on
interplay
these
two
processes.
Additionally,
article
offers
overview
targeted
drugs
shown
to
be
effective
cellular
experiments,
animal
models,
clinical
trials,
analyzing
action
potential
side
effects.
The
goal
provide
insights
for
future
drug
development
applications.
Moreover,
challenges
prospects
multi-target
combination
therapies
personalized
medicine
interventions
practice
offer
strategic
guidance
comprehensive
prevention
management
DCM.
Molecular Medicine,
Год журнала:
2025,
Номер
31(1)
Опубликована: Май 15, 2025
Abstract
Background
Retinal
degeneration
is
a
leading
cause
of
blindness
worldwide.
The
induction
ferroptosis
has
been
identified
as
an
important
mechanism
contributing
to
the
loss
photoreceptors
in
retinal
degeneration.
Lipocalin-2
(LCN2)
exhibits
iron-regulatory
properties
and
may
modulate
cell
viability
various
diseases.
However,
effects
LCN2
on
remain
unclear.
Methods
A
light-induced
injury
model
using
661W
photoreceptor
cells
male
rat
were
established.
protein
expression
was
assessed
by
western
blotting.
vitro
investigated
recombinant
(rLCN2)
small-interfering
RNA
(siRNA)
targeting
(siLCN2).
Fe
2+
,
malondialdehyde
(MDA),
tripeptide
glutathione
(GSH)
levels,
ferroptosis-associated
proteins
(solute
carrier
family
7
member
11
[SLC7A11]
peroxidase-4
[GPX4])
measured.
phosphokinase
array
blotting
performed
elucidate
mechanisms
underlying
LCN2-modulated
ferroptosis.
Additionally,
protective
knockdown
adeno-associated
virus
(AAV)-expressing
short
hairpin
(shRNA)
(AAV-shRNA-LCN2)
structure
function
vivo
evaluated
hematoxylin
eosin
staining
electroretinography.
Results
significantly
upregulated
following
light
exposure.
Treatment
with
rLCN2
induced
cells,
shown
decreased
viability,
increased
inhibition
SLC7A11
GPX4
expression,
depletion
GSH,
enhanced
MDA
whereas
siLCN2
protected
against
these
effects.
Exposure
activated
c-Jun
N-terminal
kinase
(JNK),
administration
JNK
inhibitor
SP600125
from
Lastly,
AAV-shRNA-LCN2
inhibited
retina,
vivo.
Conclusion
key
regulator
modulating
pathway.
Therefore,
presents
new
target
for
treatment
