Journal of Neuroinflammation,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: March 5, 2024
Abstract
Age-related
macular
degeneration
(AMD)
is
a
leading
cause
of
irreversible
vision
loss,
characterised
by
the
dysfunction
and
death
photoreceptors
retinal
pigment
epithelium
(RPE).
Innate
immune
cell
activation
accompanying
para-inflammation
have
been
suggested
to
contribute
pathogenesis
AMD,
although
exact
mechanism(s)
signalling
pathways
remain
elusive.
Pattern
recognition
receptors
(PRRs)
are
essential
activators
innate
system
drivers
para-inflammation.
Of
these
PRRs,
two
most
prominent
(1)
Toll-like
(TLR)
(2)
NOD-,
LRR-
pyrin
domain-containing
protein
3
(NLRP3)-inflammasome
found
modulate
progression
AMD.
Mutations
in
TLR2
be
associated
with
an
increased
risk
developing
In
animal
models
inhibition
TLR
NLRP3
has
shown
reduce
RPE
death,
inflammation
angiogenesis
signalling,
offering
potential
novel
treatments
for
advanced
Here,
we
examine
evidence
TLRs2/3/4,
NLRP3-inflammasome
pathogenesis.
Journal of Neuroscience,
Journal Year:
2020,
Volume and Issue:
40(49), P. 9364 - 9371
Published: Oct. 29, 2020
Mechanosensitivity
is
a
well-known
feature
of
astrocytes,
however,
its
underlying
mechanisms
and
functional
significance
remain
unclear.
There
evidence
that
astrocytes
are
acutely
sensitive
to
decreases
in
cerebral
perfusion
pressure
may
function
as
intracranial
baroreceptors,
tuned
monitor
brain
blood
flow.
This
study
investigated
the
mechanosensory
signaling
brainstem
these
cells
reside
alongside
cardiovascular
control
circuits
mediate
increases
heart
rate
induced
by
falls
perfusion.
It
was
found
mechanical
stimulation-evoked
Ca
2+
responses
rat
were
blocked
(1)
antagonists
connexin
channels,
43
(Cx43)
blocking
peptide
Gap26,
or
Cx43
gene
knock-down;
(2)
TRPV4
channels;
(3)
antagonist
P2Y
1
receptors
for
ATP;
(4)
inhibitors
phospholipase
C
IP3
receptors.
Proximity
ligation
assay
demonstrated
interaction
between
channels
astrocytes.
Dye
loading
experiments
showed
stimulation
increased
open
probability
carboxyfluorescein-permeable
membrane
channels.
These
data
suggest
mediated
leading
Cx43-mediated
release
ATP
which
propagates/amplifies
signals
via
recruitment
from
intracellular
stores.
In
astrocyte-specific
knock-out
mice
magnitude
acute
not
affected
deficiency.
However,
animals
displayed
lower
rates
at
different
levels
perfusion,
supporting
hypothesis
hemichannel-mediated
molecules
having
an
excitatory
action
on
CNS
sympathetic
circuits.
SIGNIFICANCE
STATEMENT
suggesting
baroreceptors
play
important
role
systemic
circulation.
To
must
possess
specialized
mechanism
makes
them
exquisitely
stimuli.
shows
opening
hemichannels
key
central
event
astroglial
plays
autonomic
rate.
add
growing
body
versatile
surveyors
metabolic
milieu,
detect
conditions
potential
threat,
such
hypoxia,
hypercapnia,
reduced
Progress in Retinal and Eye Research,
Journal Year:
2023,
Volume and Issue:
97, P. 101217 - 101217
Published: Sept. 30, 2023
Retinal
ganglion
cells,
the
neurons
that
die
in
glaucoma,
are
endowed
with
a
high
metabolism
requiring
optimal
provision
of
oxygen
and
nutrients
to
sustain
their
activity.
The
timely
regulation
blood
flow
is,
therefore,
essential
supply
firing
active
areas
glucose
they
need
for
energy.
Many
glaucoma
patients
suffer
from
vascular
deficits
including
reduced
flow,
impaired
autoregulation,
neurovascular
coupling
dysfunction,
blood-retina/brain-barrier
breakdown.
These
processes
tightly
regulated
by
community
cells
known
as
unit
comprising
neurons,
endothelial
pericytes,
Müller
astrocytes,
microglia.
In
this
review,
takes
center
stage
we
examine
ability
its
members
regulate
interactions
how
function
might
be
altered
during
glaucomatous
stress.
Pericytes
receive
special
attention
based
on
recent
data
demonstrating
key
role
physiological
pathological
conditions.
Of
particular
interest
is
discovery
characterization
tunneling
nanotubes,
thin
actin-based
conduits
connect
distal
which
play
roles
complex
spatial
temporal
distribution
within
retinal
capillary
network.
We
discuss
cellular
molecular
mechanisms
pathophysiological
implications,
while
highlighting
opportunities
develop
strategies
protection
regeneration
improve
functional
outcomes
glaucoma.
Journal of Neuroinflammation,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: March 5, 2024
Abstract
Age-related
macular
degeneration
(AMD)
is
a
leading
cause
of
irreversible
vision
loss,
characterised
by
the
dysfunction
and
death
photoreceptors
retinal
pigment
epithelium
(RPE).
Innate
immune
cell
activation
accompanying
para-inflammation
have
been
suggested
to
contribute
pathogenesis
AMD,
although
exact
mechanism(s)
signalling
pathways
remain
elusive.
Pattern
recognition
receptors
(PRRs)
are
essential
activators
innate
system
drivers
para-inflammation.
Of
these
PRRs,
two
most
prominent
(1)
Toll-like
(TLR)
(2)
NOD-,
LRR-
pyrin
domain-containing
protein
3
(NLRP3)-inflammasome
found
modulate
progression
AMD.
Mutations
in
TLR2
be
associated
with
an
increased
risk
developing
In
animal
models
inhibition
TLR
NLRP3
has
shown
reduce
RPE
death,
inflammation
angiogenesis
signalling,
offering
potential
novel
treatments
for
advanced
Here,
we
examine
evidence
TLRs2/3/4,
NLRP3-inflammasome
pathogenesis.
