Expert Review of Ophthalmology,
Journal Year:
2024,
Volume and Issue:
19(4), P. 261 - 270
Published: May 2, 2024
Introduction
Diabetic
macular
edema
(DME)
is
a
vision
threatening
accumulation
of
fluid
within
the
macula.
Current
treatments
involve
use
intravitreal
anti-vascular
endothelial
growth
factor
(anti-VEGF),
steroids,
and
laser
to
preserve
vision.
Investigative Ophthalmology & Visual Science,
Journal Year:
2024,
Volume and Issue:
65(2), P. 42 - 42
Published: Feb. 28, 2024
Müller
glia,
the
main
glial
cell
of
retina,
are
critical
for
neuronal
and
vascular
homeostasis
in
retina.
During
age-related
macular
degeneration
(AMD)
pathogenesis,
activation,
remodeling,
migrations
reported
areas
retinal
pigment
epithelial
(RPE)
degeneration,
photoreceptor
loss,
choroidal
neovascularization
(CNV)
lesions.
Despite
this
evidence
indicating
activation
localized
to
regions
AMD
it
is
unclear
whether
these
responses
contribute
pathology
or
occur
merely
as
a
bystander
effect.
In
review,
we
summarize
how
glia
affected
retinas
share
prospect
on
stress
might
directly
pathogenesis
AMD.
The
goal
review
highlight
need
future
studies
investigating
cell's
role
This
may
lead
better
understanding
pathology,
including
conversion
from
dry
wet
AMD,
which
has
no
effective
therapy
currently
shed
light
drug
intolerance
resistance
current
treatments.
Clinical and Experimental Ophthalmology,
Journal Year:
2024,
Volume and Issue:
52(4), P. 464 - 484
Published: Feb. 16, 2024
The
escalating
incidence
of
diabetes
mellitus
has
amplified
the
global
impact
diabetic
retinopathy.
There
are
known
structural
and
functional
changes
in
retina
that
precede
fundus
photography
abnormalities
which
currently
used
to
diagnose
clinical
Understanding
these
subclinical
alterations
is
important
for
effective
disease
management.
Histology
high-resolution
imaging
reveal
entire
neurovascular
unit,
comprised
retinal
vasculature,
neurons
glial
cells,
affected
disease.
Early
manifestations
seen
form
blood
flow
electroretinography
disturbances.
Structurally,
there
cellular
components
glia
neuronal
network.
On
imaging,
vessel
density
thickness
layers
observed.
How
disturbances
interact
ultimately
manifest
as
remains
elusive.
However,
this
knowledge
reveals
potential
early
therapeutic
targets
need
modalities
can
detect
a
setting.
Journal of Neuroinflammation,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: Aug. 24, 2024
Abstract
Ischemic
retinopathies
including
diabetic
retinopathy
are
major
causes
of
vision
loss.
Inner
blood-retinal
barrier
(BRB)
breakdown
with
retinal
vascular
hyperpermeability
results
in
macular
edema.
Although
dysfunction
the
neurovascular
unit
neurons,
glia,
and
cells
is
now
understood
to
underlie
this
process,
there
a
need
for
fuller
elucidation
underlying
events
BRB
ischemic
disease,
systematic
analysis
myeloid
exploration
cellular
cross-talk.
We
used
an
approach
microglia
depletion
CSF-1R
inhibitor
PLX5622
(PLX)
ischemia-reperfusion
(IR)
model.
Under
non-IR
conditions,
PLX
treatment
successfully
depleted
retina.
suppressed
microglial
activation
response
following
IR
as
well
infiltration
monocyte-derived
macrophages.
This
occurred
association
reduction
expression
chemokines
CCL2
inflammatory
adhesion
molecule
ICAM-1
.
In
addition,
was
marked
suppression
neuroinflammation
IL-1b
,
IL-6
Ptgs2
TNF-a
Angpt2
protein
that
regulates
permeability.
significantly
inner
IR,
without
appreciable
effect
on
neuronal
dysfunction.
A
translatomic
Müller
glial-specific
gene
vivo
using
Ribotag
demonstrated
strong
cell
multiple
pro-inflammatory
genes
treatment.
Co-culture
studies
activated
directly
upregulates
cell-expression
these
genes,
indicating
downstream
effector
IR.
two
types
endothelial
ability
both
compromise
EC
function.
Interestingly,
quiescent
enhanced
function
co-culture
system.
Together
demonstrates
pivotal
role
setting
ischemia-associated
disease
indicates
play
iBRB
dysregulation,
through
direct
indirect
effects,
while
glia
participate
amplifying
neuroinflammatory
cells.
International Journal of Retina and Vitreous,
Journal Year:
2024,
Volume and Issue:
10(1)
Published: Oct. 28, 2024
Abstract
One
of
the
most
common
health
concerns
disturbing
people
within
working
years
globally
is
diabetes
mellitus
(DM).
well-known
consequence
DM
vascular
damage,
which
can
manifest
as
macro-
and
microangiopathy
affecting
ocular
retina.
Therefore,
Diabetic
macular
edema
(DME)
a
major
sight-threatening
complication
diabetic
retinopathy
(DR)
worldwide.
It
prevalent
cause
significant
vision
impairment
in
patients.
Long-term
loss
be
avoided
by
following
early
DME
treatment
guidelines
everyday
life.
Hence,
there
are
various
therapeutic
approaches
for
management.
Currently,
first-line
anti-VEGF
family
drugs,
such
ranibizumab,
brolucizumab,
bevacizumab,
aflibercept.
Nevertheless,
relapses
disease,
inadequate
response,
resistance
during
therapy
still
seen
because
intricate
pathophysiological
foundation
disease.
Consequently,
an
excellent
requirement
to
advance
become
better
at
controlling
diseases
more
satisfactorily
require
fewer
treatments
overall.
We
conducted
thorough
literature
search
current
review
present
comprehensive
overview
primary
data
about
agents.
also
covered
novel
advances
management
probable
future
being
investigated
developed.
This
recommended
that
Large
clinical
trials
should
afford
sufficient
evidence
support
these
innovative
modalities.
Drug Research,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 15, 2025
Abstract
This
study
aims
to
explore
the
therapeutic
potential
of
thymoquinone
(TQ)
in
DR
by
assessing
its
effects
on
Müller
cell
apoptosis
through
modulation
miR-29b/SP1
pathway
a
diabetic
animal
model.
Healthy
C57BL/6
mice
(25
g)
were
used
study.
Retinal
samples
collected
from
both
normal
and
subjected
various
treatments:
TQ
(1
mg/kg/day),
glibenclamide
(GLB,
250
sitagliptin
(STG,
10
metformin
(MET,
5
mg/kg/day)
over
period
28
days.
The
measured
miR-29b
SP1
mRNA
levels
using
qRT-PCR.
Protein
expressions
SP1,
Bax,
bcl-2
analyzed
western
blotting,
while
Caspase-3
activity
an
ELISA
assay
kit,
annexin
V.
administration
resulted
52%
reduction
blood
glucose
levels.
Similarly,
GLB,
STG,
MET
treatments
reduced
60%,
57%,
61%,
respectively
(p<0.05).
In
addition,
upregulated
51.28%
downregulated
32.52%
Bax
protein
expression
decreased
64.99%,
Bcl-2
increased
62.92%
treatment
group
as
compared
untreated
controls.
Furthermore,
was
40.03%
with
Interestingly,
effect
inhibited
blocker
(p<0.05),
mimic
enhanced
this
effect;
associated
mitigation
retinal
cells
flow
cytometry
These
results
indicate
that
might
be
possible
option
for
via
pathway;
therefore,
playing
significant
role
mechanism
against
death.
Fluids and Barriers of the CNS,
Journal Year:
2025,
Volume and Issue:
22(1)
Published: Feb. 12, 2025
Hydrocephalus,
characterized
by
ventriculomegaly
due
to
cerebrospinal
fluid
accumulation
in
the
cerebral
ventricles,
is
a
co-morbidity
factor
several
neurodevelopmental,
psychiatric
and
neurodegenerative
diseases.
Aquaporin-4
(AQP4)
crucial
for
brain
water
homeostasis,
with
Aqp4
knockout
mice
showing
sporadic
increased
content.
Kinase
D
interacting
substrate
of
220
kDa
(Kidins220),
transmembrane
protein
involved
neuronal
survival,
synaptic
activity
neurogenesis,
controls
AQP4
levels
ependymocytes
astrocytes.
Indeed,
Kidins220
deficiency
leads
hydrocephalus
downregulating
VPS35,
key
component
retromer
complex,
targeting
lysosomal
degradation.
Importantly,
ependymal
barrier
idiopathic
normal
pressure
patients
shows
similar
downregulation
KIDINS220
AQP4.
In
addition,
pathogenic
variants
gene
are
linked
SINO
syndrome,
rare
disorder
spastic
paraplegia,
intellectual
disability,
nystagmus,
obesity
associated
ventriculomegaly.
Given
retina's
structural
functional
similarities
brain,
we
hypothesized
that
would
affect
retinal
regulation.
However,
diminished
expression
VPS35
retina
Kidins220-deficient
mice,
did
not
cause
edema
or
downregulate
Müller
cells.
Surprisingly,
there
was
an
increase
within
this
glial
cell
population.
Conversely,
optic
nerve
astrocytes
reduced,
as
observed
astrocytes,
suggesting
distinctive
adaptive
response
glia
retina.
Furthermore,
phenotypic
modifications
mice.
find
any
signs
damage
Future
studies
using
OCT
OCTA
syndrome
will
be
essential
elucidating
relationship
between
variants,
alterations,
papilledema,
visual
function.
Diabetes Obesity and Metabolism,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 21, 2025
This
retrospective
cross-sectional
study,
using
retinal
spectral-domain
optical
coherence
tomography
(SD-OCT)
scans,
investigated
obesity-related
structural
alterations
in
the
retina.
Ninety-two
eyes
of
92
healthy
asymptomatic
participants
were
categorized
into
two
groups
based
on
body
mass
index
(BMI)
measurements:
non-obese
(BMI
<
25,
45%)
and
pre-obese/obese
≥
55%)
to
compare
imaging
parameters
different
layers.
Structural
parameters,
including
thickness
volume
values,
obtained
across
distinct
layers
segmented
SD-OCT
scans.
The
nerve
fibre
layer
was
lower
high-BMI
group
than
low-BMI
(p
=
0.048).
However,
presented
significantly
higher
inner
nuclear
0.036).
In
region
analysis,
difference
prominent
superior
0.033)
inferior
0.001)
parafoveal
nasal
perifoveal
0.041)
regions,
while
changes
0.009)
regions.
A
stepwise
hierarchical
binary
logistic
regression
model,
controlling
for
age
gender,
pointed
significant
associations
regionally
decreased
increased
with
high
BMI
0.001).
Retinal
detected
between
healthy,
individuals
groups.
Besides
a
layer,
increase
BMI,
possibly
due
Müller
glia
responses
osmotic,
metabolic
inflammatory
stress,
awaiting
further
investigation.