Cancers,
Journal Year:
2021,
Volume and Issue:
13(15), P. 3670 - 3670
Published: July 22, 2021
Nuclear
protein
1
(NUPR1)
is
a
small
intrinsically
disordered
(IDP)
activated
in
response
to
various
types
of
cellular
stress,
including
endoplasmic
reticulum
(ER)
stress
and
oxidative
stress.
Reactive
oxygen
species
(ROS)
are
mainly
produced
during
mitochondrial
metabolism,
directly
impact
redox
homeostasis
Ferroptosis
ROS-dependent
programmed
cell
death
driven
by
an
iron-mediated
reaction.
Substantial
evidence
supports
maintenance
role
the
stress-inducible
NUPR1
on
cancer
metabolism
that
confers
chemotherapeutic
resistance
upregulating
function-associated
genes
antioxidant
cells.
NUPR1,
identified
as
antagonist
ferroptosis,
plays
important
reactions.
This
review
summarizes
current
knowledge
mechanism
behind
observed
function,
energy
iron
system.
The
therapeutic
potential
genetic
or
pharmacological
inhibition
also
discussed.
Understanding
system
mechanisms
its
regulation
ferroptosis
may
promote
development
more
efficacious
strategies
for
therapy.
Ecotoxicology and Environmental Safety,
Journal Year:
2023,
Volume and Issue:
253, P. 114636 - 114636
Published: Feb. 15, 2023
Silver
nanoparticles
(AgNPs)
have
become
one
of
the
most
popular
objects
study
for
past
few
decades.
The
ability
to
design
AgNPs
through
different
synthetic
methods
according
application
area
and
desired
features
is
their
advantage
in
many
applications.
Green
synthesis
silver
has
potential
methods.
Because
strong
antibacterial
activity,
been
used
a
wide
range
applications,
such
as
food
packaging
medical
products
devices.
With
increasing
AgNPs,
it
becoming
necessary
better
understanding
toxicity
mechanism
toxicity.
In
review,
we
first
describe
AgNPs.
field
then
briefly
described.
mechanisms
are
discussed.
Experimental & Molecular Medicine,
Journal Year:
2023,
Volume and Issue:
55(8), P. 1595 - 1619
Published: Aug. 23, 2023
Abstract
Mitochondria,
ubiquitous
double-membrane-bound
organelles,
regulate
energy
production,
support
cellular
activities,
harbor
metabolic
pathways,
and,
paradoxically,
mediate
cell
fate.
Evidence
has
shown
mitochondria
as
points
of
convergence
for
diverse
death-inducing
pathways
that
trigger
the
various
mechanisms
underlying
apoptotic
and
nonapoptotic
programmed
death.
Thus,
dysfunctional
eventually
lead
or
contribute
to
age-related
diseases,
such
neurodegenerative,
cardiovascular
diseases.
mitochondrion-associated
death-based
treatments
show
great
therapeutic
potential,
providing
novel
insights
in
clinical
trials.
This
review
discusses
mitochondrial
quality
control
networks
with
activity
triggered
by
stimuli
maintain
homeostasis
via
mitohormesis,
unfolded
protein
response,
mitophagy.
The
also
presents
details
on
forms
mitochondria-associated
death,
including
apoptosis,
necroptosis,
ferroptosis,
pyroptosis,
parthanatos,
paraptosis,
highlights
their
involvement
disease
pathogenesis,
collectively
suggesting
directions
further
research.
Nature Medicine,
Journal Year:
2022,
Volume and Issue:
28(4), P. 789 - 797
Published: April 1, 2022
Factor
VIII
gene
transfer
with
a
single
intravenous
infusion
of
valoctocogene
roxaparvovec
(AAV5-hFVIII-SQ)
has
demonstrated
clinical
benefits
lasting
5
years
to
date
in
people
severe
hemophilia
A.
Molecular
mechanisms
underlying
sustained
AAV5-hFVIII-SQ-derived
FVIII
expression
have
not
been
studied
humans.
In
substudy
the
phase
1/2
trial
(
NCT02576795
),
liver
biopsy
samples
were
collected
2.6-4.1
after
from
five
participants.
Primary
objectives
examine
effects
on
histopathology,
determine
transduction
pattern
and
percentage
hepatocytes
transduced
AAV5-hFVIII-SQ
genomes,
characterize
quantify
episomal
forms
vector
DNA
transgene
(hFVIII-SQ
RNA
hFVIII-SQ
protein).
Histopathology
revealed
no
dysplasia,
architectural
distortion,
fibrosis
or
chronic
inflammation,
endoplasmic
reticulum
stress
was
detected
expressing
protein.
Hepatocytes
stained
positive
for
showing
trend
more
cells
higher
doses.
analysis
presence
full-length,
inverted
terminal
repeat-fused,
circular
which
are
associated
long-term
expression.
Interindividual
differences
noted
despite
similar
successful
transduction,
possibly
influenced
by
host-mediated
post-transduction
transcription,
protein
translation
secretion.
Overall,
these
results
demonstrate
persistent
structures
following
administration
begin
elucidate
potential
mediating
interindividual
variability.
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.
Antioxidants,
Journal Year:
2023,
Volume and Issue:
12(5), P. 981 - 981
Published: April 22, 2023
Oxidative
stress
is
caused
by
an
imbalance
in
cellular
redox
state
due
to
the
accumulation
of
reactive
oxygen
species
(ROS).
While
homeostatic
levels
ROS
are
important
for
cell
physiology
and
signaling,
excess
can
induce
a
variety
negative
effects
ranging
from
damage
biological
macromolecules
death.
Additionally,
oxidative
disrupt
function
redox-sensitive
organelles
including
mitochondria
endoplasmic
reticulum
(ER).
In
case
ER,
misfolded
proteins
arise
stress,
leading
onset
ER
stress.
To
combat
cells
initiate
highly
conserved
response
called
unfolded
protein
(UPR).
UPR
within
context
resolving
well
characterised,
how
mediators
respond
influence
less
defined.
this
review,
we
evaluate
interplay
between
signaling
networks.
Specifically,
assess
antioxidant
responses.
Translational Neurodegeneration,
Journal Year:
2023,
Volume and Issue:
12(1)
Published: April 14, 2023
Abstract
Redox
homeostasis
refers
to
the
balance
between
production
of
reactive
oxygen
species
(ROS)
as
well
nitrogen
(RNS),
and
their
elimination
by
antioxidants.
It
is
linked
all
important
cellular
activities
oxidative
stress
a
result
imbalance
pro-oxidants
antioxidant
species.
Oxidative
perturbs
many
activities,
including
processes
that
maintain
integrity
DNA.
Nucleic
acids
are
highly
therefore
particularly
susceptible
damage.
The
DNA
damage
response
detects
repairs
these
lesions.
Efficient
repair
essential
for
maintaining
viability,
but
they
decline
considerably
during
aging.
deficiencies
in
increasingly
described
age-related
neurodegenerative
diseases,
such
Alzheimer’s
disease,
Parkinson’s
amyotrophic
lateral
sclerosis
Huntington’s
disease.
Furthermore,
has
long
been
associated
with
conditions.
Moreover,
both
redox
dysregulation
increase
significantly
aging,
which
biggest
risk
factor
diseases.
However,
links
dysfunction
damage,
joint
contributions
pathophysiology
conditions,
only
just
emerging.
This
review
will
discuss
associations
address
increasing
evidence
an
major
source
disorders.
Understanding
connections
may
facilitate
better
understanding
disease
mechanisms,
ultimately
lead
design
therapeutic
strategies
based
on
preventing
Cell Death and Disease,
Journal Year:
2024,
Volume and Issue:
15(2)
Published: Feb. 20, 2024
Abstract
Traumatic
brain
injury
(TBI)
is
a
common
trauma
with
high
mortality
and
disability
rates
worldwide.
However,
the
current
management
of
this
disease
still
unsatisfactory.
Therefore,
it
necessary
to
investigate
pathophysiological
mechanisms
TBI
in
depth
improve
treatment
options.
In
recent
decades,
abundant
evidence
has
highlighted
significance
endoplasmic
reticulum
stress
(ERS)
advancing
central
nervous
system
(CNS)
disorders,
including
TBI.
ERS
following
leads
accumulation
unfolded
proteins,
initiating
protein
response
(UPR).
Protein
kinase
RNA-like
ER
(PERK),
inositol-requiring
1
(IRE1),
activating
transcription
factor
6
(ATF6)
are
three
major
pathways
UPR
initiation
that
determine
whether
cell
survives
or
dies.
This
review
focuses
on
dual
effects
discusses
underlying
mechanisms.
It
suggested
may
crosstalk
series
molecular
cascade
responses,
such
as
mitochondrial
dysfunction,
oxidative
stress,
neuroinflammation,
autophagy,
death,
thus
involved
progression
secondary
after
Hence,
promising
candidate
for