Redox Biology,
Journal Year:
2023,
Volume and Issue:
68, P. 102967 - 102967
Published: Nov. 18, 2023
Oxidative
stress
occurs
through
an
imbalance
between
the
generation
of
reactive
oxygen
species
(ROS)
and
antioxidant
defense
mechanisms
cells.
The
eye
is
particularly
exposed
to
oxidative
because
its
permanent
exposure
light
due
several
structures
having
high
metabolic
activities.
anterior
part
highly
ultraviolet
(UV)
radiation
possesses
a
complex
system
protect
retina
from
UV
radiation.
posterior
exhibits
rates
consumption
leading
subsequently
production
rate
ROS.
Furthermore,
inflammation,
aging,
genetic
factors,
environmental
pollution,
are
all
elements
promoting
ROS
impairing
thereby
representing
risk
factors
stress.
An
abnormal
redox
status
was
shown
be
involved
in
pathophysiology
various
ocular
diseases
segment
eye.
In
this
review,
we
aim
summarize
provide
updated
understanding
on
pathogenesis
common
affecting
surface,
lens,
retina,
optic
nerve.
Moreover,
discuss
potential
therapeutic
approaches
aimed
at
reducing
context.
Metabolites,
Journal Year:
2023,
Volume and Issue:
13(2), P. 187 - 187
Published: Jan. 27, 2023
Redox
homeostasis
is
a
delicate
balancing
act
of
maintaining
appropriate
levels
antioxidant
defense
mechanisms
and
reactive
oxidizing
oxygen
nitrogen
species.
Any
disruption
this
balance
leads
to
oxidative
stress,
which
key
pathogenic
factor
in
several
ocular
diseases.
In
review,
we
present
the
current
evidence
for
stress
mitochondrial
dysfunction
conditions
affecting
both
anterior
segment
(e.g.,
dry
eye
disease,
keratoconus,
cataract)
posterior
(age-related
macular
degeneration,
proliferative
vitreoretinopathy,
diabetic
retinopathy,
glaucoma)
human
eye.
We
posit
that
further
development
therapeutic
interventions
promote
pro-regenerative
responses
maintenance
redox
may
delay
or
prevent
progression
these
major
pathologies.
Continued
efforts
field
will
not
only
yield
better
understanding
molecular
underlying
pathogenesis
diseases
but
also
enable
identification
novel
druggable
targets
therapies.
Molecular Neurodegeneration,
Journal Year:
2022,
Volume and Issue:
17(1)
Published: March 28, 2022
Abstract
Background
The
retina,
as
part
of
the
central
nervous
system
(CNS)
with
limited
capacity
for
self-reparation
and
regeneration
in
mammals,
is
under
cumulative
environmental
stress
due
to
high-energy
demands
rapid
protein
turnover.
These
stressors
disrupt
cellular
metabolic
homeostasis,
which,
if
not
alleviated,
can
lead
dysfunction
cell
death
retinal
neurons.
One
primary
response
highly
conserved
unfolded
(UPR).
UPR
acts
through
three
main
signaling
pathways
an
attempt
restore
homeostasis
endoplasmic
reticulum
(ER)
by
various
means,
including
but
to,
reducing
translation,
increasing
protein-folding
capacity,
promoting
misfolded
degradation.
Moreover,
recent
work
has
identified
a
novel
function
regulation
metabolism
mitochondrial
function,
disturbance
which
contributes
neuronal
degeneration
dysfunction.
role
neurons
during
aging
disease
conditions
age-related
macular
(AMD),
retinitis
pigmentosa
(RP),
glaucoma,
diabetic
retinopathy
(DR)
been
explored
over
past
two
decades.
Each
their
corresponding
animal
models
provide
distinct
challenges
unique
opportunities
gain
better
understanding
maintenance
health
function.
Method
We
performed
extensive
literature
search
on
PubMed
Google
Scholar
using
following
keywords:
response,
metabolism,
ER
stress,
degeneration,
aging,
pigmentosa,
retinopathy.
Results
conclusion
summarize
advances
particular
UPR,
diseases,
highlighting
potential
roles
Further,
we
perspective
promise
targeting
new
therapeutic
approach
age-
disease-related
degeneration.
Frontiers in Physiology,
Journal Year:
2023,
Volume and Issue:
14
Published: July 12, 2023
Periodontitis
is
a
common
inflammatory
disease.
It
characterized
by
destruction
of
the
supporting
structures
teeth
and
could
lead
to
tooth
loss
systemic
inflammation.
Bacteria
in
inflamed
gingival
tissue
virulence
factors
are
capable
entering
bloodstream
induce
response,
thus
influencing
pathological
process
many
diseases,
such
as
cardiovascular
diabetes,
chronic
kidney
disease,
well
liver
injury.
An
increasing
body
evidence
show
complex
interplay
between
oxidative
stress
inflammation
disease
pathogenesis.
When
periodontitis
occurs,
increased
reactive
oxygen
species
accumulation
leads
stress.
Oxidative
contributes
major
cellular
components
damage,
including
DNA,
proteins,
lipids.
In
this
article,
focus
will
be
on
periodontal
relationship
inflammation,
impact
therapy
parameters.
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.
Aging and Disease,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Jan. 1, 2024
Age-related
macular
degeneration
(AMD)
is
a
prevalent
degenerative
disorder
of
the
central
retina,
which
holds
global
significance
as
fourth
leading
cause
blindness.
The
condition
characterized
by
multifaceted
pathophysiology
that
involves
aging,
oxidative
stress,
inflammation,
vascular
dysfunction,
and
complement
activation.
complex
interplay
these
factors
contributes
to
initiation
progression
AMD.
Current
treatments
primarily
address
choroidal
neovascularization
(CNV)
in
neovascular
However,
approval
novel
drug
therapies
for
atrophic
more
gradual
variant,
known
geographic
atrophy
(GA),
has
recently
occurred.
In
light
substantial
impact
AMD
on
affected
individuals'
quality
life
strain
it
places
healthcare
systems,
there
pressing
need
innovative
medications.
This
paper
aims
provide
an
updated
comprehensive
overview
advancements
our
understanding
etiopathogenesis
Special
attention
will
be
given
influence
aging
altered
redox
status
mitochondrial
dynamics,
cell
death
pathways,
intricate
between
stress
system,
specifically
context
GA.
Additionally,
this
review
shed
newly
approved
explore
emerging
alternative
treatment
strategies
field.
objective
contribute
ongoing
dialogue
surrounding
AMD,
offering
insights
into
latest
developments
may
pave
way
effective
management
intervention
approaches.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(8), P. 4158 - 4158
Published: April 9, 2024
Age-related
macular
degeneration
(AMD)
is
a
chronic
disease
that
usually
develops
in
older
people.
Pathogenetic
changes
this
include
anatomical
and
functional
complexes.
Harmful
factors
damage
the
retina
macula.
These
may
lead
to
partial
or
total
loss
of
vision.
The
can
occur
two
clinical
forms:
dry
(the
progression
slow
gentle)
exudative
(wet—progression
acute
severe),
which
starts
form;
however,
coexistence
both
forms
possible.
etiology
AMD
not
fully
understood,
precise
mechanisms
development
illness
are
still
unknown.
Extensive
genetic
studies
have
shown
multi-factorial
determinants,
along
with
external
internal
environmental
metabolic-functional
factors,
important
risk
factors.
This
article
reviews
role
glutathione
(GSH)
enzymes
engaged
maintaining
reduced
form
polymorphism
S-transferase
theta-1
(GSTT1)
mu-1
(GSTM1)
AMD.
We
only
chose
papers
confirmed
influence
parameters
on
Because
GSH
most
antioxidant
eye,
it
know
background
ensure
an
optimal
level
concentration.
Numerous
been
conducted
how
system
works
till
today.
paper
presents
current
state
knowledge
about
GSH,
GST,
GR,
GPx
GST
clearly
show
increased
activity
ill
people,
but
for
GPx,
results
relating
so
clear.
Depending
research,
also
suggest
higher
lower
patients
analysis
polymorphisms
genes
mutations
weaker
barriers
contribute
AMD;
unfortunately,
meta-analysis
some
research
did
confirm
connection.
Unspecific
many
make
up
unknowns.
It
conduct
further
understand
exact
mechanism
defense
functions
against
oxidative
stress
human
eye.
Antioxidants,
Journal Year:
2025,
Volume and Issue:
14(2), P. 152 - 152
Published: Jan. 27, 2025
Age-related
macular
degeneration
(AMD)
is
a
leading
cause
of
vision
impairment
worldwide,
primarily
driven
by
oxidative
stress
and
inflammation.
This
review
examines
the
role
antioxidants
in
mitigating
damage,
emphasizing
both
their
therapeutic
potential
limitations
AMD
management.
Key
findings
underscore
efficacy
specific
antioxidants,
including
vitamins
C
E,
lutein,
zeaxanthin,
Coenzyme
Q10,
slowing
progression.
Landmark
studies
such
as
AREDS
AREDS2
have
shaped
current
antioxidant
formulations,
although
challenges
persist,
patient
variability
long-term
safety
concerns.
Emerging
therapies,
mitochondrial-targeted
novel
compounds
like
saffron
resveratrol,
offer
promising
avenues
for
treatment.
Complementary
lifestyle
interventions,
antioxidant-rich
diets
physical
activity,
further
support
holistic
management
approaches.
highlights
critical
therapy,
advocating
personalized
strategies
to
optimize
outcomes.
Antioxidants,
Journal Year:
2021,
Volume and Issue:
10(5), P. 653 - 653
Published: April 23, 2021
Although
the
exact
pathogenetic
mechanisms
leading
to
age-related
macular
degeneration
(AMD)
have
not
been
clearly
identified,
oxidative
damage
in
retina
and
choroid
due
an
imbalance
between
local
oxidants/anti-oxidant
systems
chronic
inflammation
could
represent
trigger
event.
Different
vitro
vivo
models
demonstrated
involvement
of
reactive
oxygen
species
generated
a
highly
environment
development
drusen
retinal
pigment
epithelium
(RPE)
changes
initial
pathologic
processes
AMD;
moreover,
recent
evidence
has
highlighted
possible
association
stress
neovascular
AMD.
Nitric
oxide
(NO),
which
is
known
play
key
role
physiological
regulation
choroidal
blood
flow,
under
conditions
lead
RPE/photoreceptor
generation
peroxynitrite,
potentially
cytotoxic
tyrosine-nitrating
molecule.
Furthermore,
altered
expression
different
isoforms
NO
synthases
be
involved
microvascular
neovascularization.
The
purpose
this
review
was
investigate
pathways
activated
by
oxidative/nitrosative
pathogenesis
AMD,
focusing
on
neovascularization
protective
anti-vascular
endothelial
growth
factor
agents
context.