Journal of Nanobiotechnology,
Год журнала:
2024,
Номер
22(1)
Опубликована: Март 26, 2024
Abstract
Background
Cardiovascular
diseases
(CVDs)
have
the
highest
mortality
worldwide.
Human
pluripotent
stem
cells
(hPSCs)
and
their
cardiomyocyte
derivatives
(hPSC-CMs)
offer
a
valuable
resource
for
disease
modeling,
pharmacological
screening,
regenerative
therapy.
While
most
CVDs
are
linked
to
significant
over-production
of
reactive
oxygen
species
(ROS),
effects
current
antioxidants
targeting
excessive
ROS
limited.
Nanotechnology
is
powerful
tool
develop
with
improved
selectivity,
solubility,
bioavailability
prevent
or
treat
various
related
oxidative
stress.
Cerium
oxide
nanozymes
(CeONZs)
can
effectively
scavenge
by
mimicking
activity
endogenous
antioxidant
enzymes.
This
study
aimed
assess
nanotoxicity
CeONZs
potential
benefits
in
stressed
human
embryonic
(hESCs)
derived
cardiomyocytes
(hESC-CMs).
Results
demonstrated
reliable
nanosafety
biocompatibility
hESCs
hESC-CMs
within
broad
range
concentrations.
exhibited
protective
on
cell
viability
alleviating
ROS-induced
Moreover,
protected
from
doxorubicin
(DOX)-induced
cardiotoxicity
partially
ameliorated
insults
DOX
neonatal
rat
(NRCMs).
Furthermore,
during
culture,
were
found
reduce
ROS,
decrease
apoptosis,
enhance
survival
without
affecting
self-renewal
differentiation
potential.
Conclusions
displayed
good
safety
biocompatibility,
as
well
enhanced
shielding
them
damage.
These
promising
results
suggest
that
may
be
crucial,
safe
nanoantioxidant,
potentially
improve
therapeutic
efficacy
incorporated
into
medicine.
Graphical
Cells,
Год журнала:
2023,
Номер
12(9), С. 1341 - 1341
Опубликована: Май 8, 2023
Reactive
oxygen
species
(ROS)
are
radical
intermediates
that
serve
as
important
second
messengers
in
signal
transduction.
However,
when
the
accumulation
of
these
molecules
exceeds
buffering
capacity
antioxidant
enzymes,
oxidative
stress
and
endothelial
cell
(EC)
dysfunction
occur.
EC
shifts
vascular
system
into
a
pro-coagulative,
proinflammatory
state,
thereby
increasing
risk
developing
cardiovascular
(CV)
diseases
metabolic
disorders.
Studies
have
turned
to
investigation
microRNA
treatment
for
CV
factors,
post-transcription
regulators
known
co-regulate
ROS.
In
this
review,
we
will
discuss
ROS
pathways
generation,
normal
physiology
ROS-induced
dysfunction,
current
knowledge
common
disorders
their
connection
stress.
Therapeutic
strategies
based
on
microRNAs
response
microRNA’s
regulatory
roles
controlling
also
be
explored.
It
is
gain
an
in-depth
comprehension
mechanisms
generating
how
manipulating
enzymatic
byproducts
can
protect
function
from
prevent
development
Antioxidants,
Год журнала:
2023,
Номер
12(3), С. 778 - 778
Опубликована: Март 22, 2023
Neurodegenerative
diseases
are
incurable
and
debilitating
conditions
that
result
in
progressive
degeneration
loss
of
nerve
cells.
Oxidative
stress
has
been
proposed
as
one
factor
plays
a
potential
role
the
pathogenesis
neurodegenerative
disorders
since
neuron
cells
particularly
vulnerable
to
oxidative
damage.
Nuclear
(erythroid-derived
2)-like
2
(Nrf2)
is
strictly
related
anti-inflammatory
antioxidative
cell
response;
therefore,
its
activation
consequent
enhancement
cellular
pathways
have
therapeutic
approach.
Several
Nrf2
activators
with
different
mechanisms
diverse
structures
reported,
but
those
applied
for
neurodisorders
still
limited.
However,
very
last
few
years,
interesting
progress
made,
enhancing
blood–brain
barrier
penetration,
make
effective
drugs,
designing
Nrf2-based
multitarget-directed
ligands
affect
multiple
involved
pathology
diseases.
The
present
review
gives
an
overview
most
representative
findings
this
research
area.
Cell Host & Microbe,
Год журнала:
2024,
Номер
32(6), С. 852 - 862
Опубликована: Июнь 1, 2024
Antibiotic
resistance,
typically
associated
with
genetic
changes
within
a
bacterial
population,
is
frequent
contributor
to
antibiotic
treatment
failures.
persistence
and
tolerance,
which
we
collectively
term
recalcitrance,
represent
transient
phenotypic
in
the
population
that
prolong
survival
presence
of
lethal
concentrations
antibiotics.
recalcitrance
challenging
detect
investigate-traditionally
studied
under
vitro
conditions,
our
understanding
during
infection
its
contribution
failure
limited.
Recently,
significant
progress
has
been
made
study
antibiotic-recalcitrant
populations
pathogenic
species,
including
Mycobacterium
tuberculosis,
Staphylococcus
aureus,
Salmonella
enterica,
Yersiniae,
context
host
environment.
Despite
diversity
these
pathogens
models,
shared
signals
responses
promote
common
features
vulnerabilities
persisters
tolerant
bacteria
have
emerged.
These
will
be
discussed
here,
along
toward
developing
therapeutic
interventions
better
treat
recalcitrant
pathogens.
PLoS Biology,
Год журнала:
2024,
Номер
22(5), С. e3002299 - e3002299
Опубликована: Май 7, 2024
Activation
of
immune
cells
requires
the
remodeling
cell
metabolism
in
order
to
support
function.
We
study
these
metabolic
changes
through
infection
Drosophila
larvae
by
parasitoid
wasp.
The
egg
is
neutralized
differentiating
lamellocytes,
which
encapsulate
egg.
A
melanization
cascade
initiated,
producing
toxic
molecules
destroy
while
capsule
also
protects
host
from
reaction.
combined
transcriptomics
and
metabolomics,
including
13
C-labeled
glucose
trehalose
tracing,
as
well
genetic
manipulation
sugar
metabolism,
specifically
hemocytes.
found
that
hemocytes
increase
expression
several
carbohydrate
transporters
accordingly
uptake
more
during
infection.
These
carbohydrates
are
metabolized
increased
glycolysis,
associated
with
lactate
production,
cyclic
pentose
phosphate
pathway
(PPP),
glucose-6-phosphate
re-oxidized
maximize
NADPH
yield.
Oxidative
PPP
required
for
lamellocyte
differentiation
resistance,
systemic
metabolism.
In
addition,
fully
differentiated
lamellocytes
use
a
cytoplasmic
form
trehalase
cleave
fuel
PPP.
Intracellular
not
differentiation,
but
its
down-regulation
elevates
levels
reactive
oxygen
species,
resistance
reduced
fitness.
Our
results
suggest
PPP,
within
important
only
fight
protect
own
response
ensuring
fitness
survivor.
Antioxidants,
Год журнала:
2025,
Номер
14(3), С. 264 - 264
Опубликована: Фев. 25, 2025
Autophagy
is
a
fundamental
cellular
process
that
maintains
homeostasis
by
degrading
damaged
components
and
regulating
stress
responses.
It
plays
crucial
role
in
cancer
biology,
including
tumor
progression,
metastasis,
therapeutic
resistance.
Oxidative
stress,
similarly,
key
to
maintaining
balance
oxidants
antioxidants,
with
its
disruption
leading
molecular
damage.
The
interplay
between
autophagy
oxidative
particularly
significant,
as
reactive
oxygen
species
(ROS)
act
both
inducers
by-products
of
autophagy.
While
can
function
suppressor
early
stages,
it
often
shifts
pro-tumorigenic
advanced
disease,
aiding
cell
survival
under
adverse
conditions
such
hypoxia
nutrient
deprivation.
This
dual
mediated
several
signaling
pathways,
PI3K/AKT/mTOR,
AMPK,
HIF-1α,
which
coordinate
the
autophagic
activity
ROS
production.
In
this
review,
we
explore
mechanisms
interact
across
different
hematological
malignancies.
We
discuss
how
triggers
autophagy,
creating
feedback
loop
promotes
survival,
dysregulation
leads
increased
accumulation,
exacerbating
tumorigenesis.
also
examine
implications
targeting
autophagy-oxidative
axis
cancer.
Current
strategies
involve
modulating
through
specific
inhibitors,
enhancing
levels
pro-oxidant
compounds,
combining
these
approaches
conventional
therapies
overcome
drug
Understanding
complex
relationship
provides
critical
insights
into
novel
aimed
at
improving
treatment
outcomes.
Nature Metabolism,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 14, 2025
Animals
select
food
based
on
hungers
that
reflect
dynamic
macronutrient
needs,
but
the
hormonal
mechanisms
underlying
nutrient-specific
appetite
regulation
remain
poorly
defined.
Here,
we
identify
tachykinin
(Tk)
as
a
protein-responsive
gut
hormone
in
Drosophila
and
female
mice,
regulated
by
conserved
environmental
nutrient-sensing
mechanisms.
Protein
intake
activates
Tk-expressing
enteroendocrine
cells
(EECs),
driving
release
of
Tk
through
involving
target
rapamycin
(TOR)
transient
receptor
potential
A1
(TrpA1).
In
flies,
delineate
pathway
which
controls
selective
sleep
after
protein
ingestion,
mediated
glucagon-like
adipokinetic
(AKH)
signalling
to
neurons
adipose
tissue.
This
mechanism
suppresses
appetite,
promotes
sugar
hunger
modulates
wakefulness
align
behaviour
with
nutritional
needs.
Inhibiting
prolongs
lifespan
AKH,
revealing
role
for
nutrient-dependent
longevity.
Our
results
provide
framework
understanding
EEC-derived
satiety
signals
hormones
regulating
choice,
lifespan.
Nutrients,
Год журнала:
2023,
Номер
15(10), С. 2283 - 2283
Опубликована: Май 12, 2023
This
review
aims
to
discuss
the
delicate
balance
between
physiological
production
of
reactive
oxygen
species
and
role
antioxidant
nutraceutical
molecules
in
managing
radicals
complex
anatomical
structure
eye.
Many
enzymes
with
reducing
potential
are
present
different
parts
Some
these,
such
as
glutathione,
N-acetylcysteine,
α-lipoic
acid,
coenzyme
Q10,
enzymatic
antioxidants,
endogenously
produced
by
body.
Others,
plant-derived
polyphenols
carotenoids,
vitamins
B2,
C,
E,
zinc
selenium,
omega-3
polyunsaturated
fatty
acids,
must
be
obtained
through
diet
considered
essential
nutrients.
When
equilibrium
their
scavenging
is
disrupted,
radical
generation
overwhelms
endogenous
arsenal,
leading
oxidative
stress-related
eye
disorders
aging.
Therefore,
roles
antioxidants
contained
dietary
supplements
preventing
stress-based
ocular
dysfunctions
also
discussed.
However,
results
studies
investigating
efficacy
supplementation
have
been
mixed
or
inconclusive,
indicating
a
need
for
future
research
highlight
develop
new
preventive
nutritional
strategies.