Biomolecules,
Год журнала:
2023,
Номер
13(3), С. 549 - 549
Опубликована: Март 17, 2023
Alzheimer’s
disease
(AD)
is
a
common
neurodegenerative
disorder
that
affects
the
elderly.
One
of
key
features
AD
accumulation
reactive
oxygen
species
(ROS),
which
leads
to
an
overall
increase
in
oxidative
damage.
The
nuclear
factor
(erythroid-derived
2)-like
2
(Nrf2)
master
regulator
antioxidant
response
cells.
Under
low
ROS
levels,
Nrf2
kept
cytoplasm.
However,
production
translocation
into
nucleus,
where
it
activates
transcription
several
genes
involved
cells’
response.
Additionally,
activation
increases
autophagy
function.
AD,
Aβ
and
tau
reduces
decreasing
reduced
levels
contribute
further
by
impairing
their
autophagy-mediated
turnover.
In
this
review,
we
discuss
overwhelming
evidence
indicating
genetic
or
pharmacological
as
potential
approach
mitigate
pathology.
Antioxidants,
Год журнала:
2022,
Номер
11(3), С. 538 - 538
Опубликована: Март 11, 2022
In
a
multicellular
environment,
many
different
types
of
cells
interact
with
each
other.
The
KEAP1-NRF2
system
defends
against
electrophilic
and
oxidative
stresses
in
various
cells.
However,
the
also
regulates
expression
genes
involved
cell
proliferation
inflammation,
indicating
that
plays
type-specific
roles.
this
review,
we
introduce
multifarious
roles
cells,
especially
focusing
on
cancer
inflammatory
diseases.
Cancer
frequently
hijack
system,
NRF2
activation
confers
proliferative
advantage
therapeutic
resistance.
contrast,
immune
myeloid
suppresses
tumor
development.
chronic
diseases,
such
as
sickle
disease,
endothelial
represses
proinflammatory
cytokine
adherent
molecule
genes,
mitigating
inflammation
organ
damage.
Based
these
cell-specific
played
by
inducers
have
been
utilized
for
treatment
addition,
use
and/or
inhibitors
canonical
antineoplastic
drugs
is
an
emerging
approach
to
treatment.
Redox Biology,
Год журнала:
2023,
Номер
60, С. 102624 - 102624
Опубликована: Фев. 2, 2023
NF-E2-related
factor
2
(NRF2)
plays
a
crucial
role
in
the
maintenance
of
cellular
homeostasis
by
regulating
various
enzymes
and
proteins
that
are
involved
redox
reactions
utilizing
sulfur.
While
substantial
impacts
NRF2
on
mitochondrial
activity
have
been
described,
precise
mechanism
which
regulates
function
is
still
not
fully
understood.
Here,
we
demonstrated
increased
intracellular
persulfides
upregulating
cystine
transporter
xCT
encoded
Slc7a11,
well-known
target
gene.
Persulfides
shown
to
play
an
important
function.
Supplementation
with
glutathione
trisulfide
(GSSSG),
form
persulfide,
elevated
membrane
potential
(MMP),
oxygen
consumption
rate
(OCR)
promoted
ATP
production.
Persulfide-mediated
activation
was
require
sulfur
oxidation
pathway,
especially
sulfide
quinone
oxidoreductase
(SQOR).
Consistently,
NRF2-mediated
also
dependent
SQOR
activity.
This
study
clarified
facilitation
persulfide
production
metabolism
mitochondria
increasing
cysteine
availability
one
mechanisms
for
NRF2-dependent
activation.
British Journal of Pharmacology,
Год журнала:
2023,
Номер
unknown
Опубликована: Сен. 16, 2023
The
KEAP1
‐
NRF2
system
plays
a
central
role
in
cytoprotection
defence
mechanisms
against
oxidative
stress.
KEAP1‐NRF2
has
been
regarded
as
sulfur‐utilizing
cytoprotective
mechanism,
because
serves
biosensor
for
electrophiles
by
using
its
reactive
thiols
and
is
transcriptional
factor
regulating
genes
involved
sulfur‐mediated
redox
reactions.
key
regulator
of
genes,
such
antioxidant
detoxification
also
possesses
potent
anti‐inflammatory
activity.
Recently
the
focus
attention
cellular
metabolism
mitochondrial
function.
NRF2‐mediated
regulatory
metabolites
mitochondria
have
considered
diverse,
but
not
yet
fully
clarified.
This
review
article
provides
an
overview
molecular
that
regulate
signalling
roles,
highlights
contribution
to
metabolism,
particularly
context
function
newly‐found
sulfur
metabolism.
Biomolecules,
Год журнала:
2023,
Номер
13(3), С. 549 - 549
Опубликована: Март 17, 2023
Alzheimer’s
disease
(AD)
is
a
common
neurodegenerative
disorder
that
affects
the
elderly.
One
of
key
features
AD
accumulation
reactive
oxygen
species
(ROS),
which
leads
to
an
overall
increase
in
oxidative
damage.
The
nuclear
factor
(erythroid-derived
2)-like
2
(Nrf2)
master
regulator
antioxidant
response
cells.
Under
low
ROS
levels,
Nrf2
kept
cytoplasm.
However,
production
translocation
into
nucleus,
where
it
activates
transcription
several
genes
involved
cells’
response.
Additionally,
activation
increases
autophagy
function.
AD,
Aβ
and
tau
reduces
decreasing
reduced
levels
contribute
further
by
impairing
their
autophagy-mediated
turnover.
In
this
review,
we
discuss
overwhelming
evidence
indicating
genetic
or
pharmacological
as
potential
approach
mitigate
pathology.
