Antioxidants and Redox Signaling,
Год журнала:
2023,
Номер
41(13-15), С. 845 - 864
Опубликована: Дек. 8, 2023
Significance:
The
growing
importance
of
mitochondria
in
the
immune
response
and
inflammation
is
multifaceted.
Unraveling
different
mechanisms
by
which
have
a
relevant
role
inflammatory
beyond
energy
management
process
necessary
for
improving
our
understanding
host
defense
pathogenesis
various
diseases
syndromes.
Critical
Issues:
Mitochondria
are
at
levels,
including
releasing
activation
molecules,
changing
its
structure
function
to
accompany
response,
serving
as
structural
base
activating
intermediates
NLRP3
inflammasome.
In
this
scientific
journey
dissecting
mitochondrial
mechanisms,
new
questions
interesting
aspects
arise,
such
involvement
mitochondrial-derived
vesicles
with
putative
preventing
uncontrolled
situations.
Recent
Advances:
Researchers
continuously
rethinking
acute
chronic
related
disorders.
As
such,
important
roles
centrally
positioned
signaling
hubs
regulating
responses.
review,
we
present
current
involved,
largely
known
dysfunction,
onset
development
Future
Directions:
emerge
an
multifaceted
platform
studying
developing
pharmaceutical
therapeutic
approaches.
There
many
ongoing
studies
aimed
describe
effects
specific
targeted
molecules
treatments
ameliorate
consequences
exacerbated
components
pathologies
syndromes,
resulting
open
area
increasing
research
interest.
Expert Opinion on Therapeutic Targets,
Год журнала:
2023,
Номер
27(10), С. 939 - 952
Опубликована: Сен. 22, 2023
Drugs
targeting
mitochondria
are
emerging
as
promising
antitumor
therapeutics
in
preclinical
models.
However,
a
few
of
these
drugs
have
shown
clinical
toxicity.
Developing
mitochondria-targeted
modified
natural
compounds
and
US
FDA-approved
with
increased
therapeutic
index
cancer
is
discussed
an
alternative
strategy.
Advanced Materials,
Год журнала:
2023,
Номер
unknown
Опубликована: Сен. 4, 2023
Neoadjuvant
and
adjuvant
therapies
have
made
significant
progress
in
cancer
treatment.
However,
tumor
therapy
still
faces
challenges
due
to
the
intrinsic
heterogeneity
of
cancer,
genomic
instability,
formation
an
immunosuppressive
microenvironment.
Functional
materials
possess
unique
biological
properties
such
as
long
circulation
times,
tumor-specific
targeting,
immunomodulation.
The
combination
functional
with
natural
substances
nanotechnology
has
led
development
smart
biomaterials
multiple
functions,
high
biocompatibilities,
negligible
immunogenicities,
which
can
be
used
for
precise
Recently,
subcellular
structure-targeting
received
particular
attention
various
biomedical
applications
including
diagnosis,
sensing,
imaging
tumors
drug
delivery.
Subcellular
organelle-targeting
precisely
accumulate
therapeutic
agents
organelles,
considerably
reduce
threshold
dosages
agents,
minimize
drug-related
side
effects.
This
review
provides
a
systematic
comprehensive
overview
research
organelle-targeted
based
on
nanomaterials.
Moreover,
it
explains
prospects
precision
oncology.
will
serve
excellent
cutting-edge
guide
researchers
field
therapy.
World Journal of Gastroenterology,
Год журнала:
2024,
Номер
30(7), С. 714 - 727
Опубликована: Фев. 21, 2024
BACKGROUND
Pancreatic
cancer
is
a
leading
cause
of
cancer-related
deaths.
Increased
activity
the
epidermal
growth
factor
receptor
(EGFR)
often
observed
in
pancreatic
cancer,
and
small
molecule
EGFR
inhibitor
erlotinib
has
been
approved
for
therapy
by
food
drug
administration.
Nevertheless,
alone
ineffective
should
be
combined
with
other
drugs
to
improve
therapeutic
outcomes.
We
previously
showed
that
certain
tyrosine
kinase
inhibitors
can
increase
mitochondrial
membrane
potential
(Δψm),
facilitate
tumor
cell
uptake
Δψm-sensitive
agents,
disrupt
homeostasis,
subsequently
trigger
death.
Erlotinib
not
tested
this
effect.
AIM
To
determine
whether
elevate
Δψm
triggering
METHODS
fluorescent
dye
was
used
how
affects
adenocarcinoma
(PDAC)
lines.
The
viability
conventional
patient-derived
primary
PDAC
lines
2D-
3D
cultures
measured
after
treating
cells
sequentially
mitochondria-targeted
ubiquinone
(MitoQ),
MitoQ.
synergy
between
MitoQ
then
analyzed
using
SynergyFinder
2.0.
preclinical
efficacy
two-drug
combination
determined
immune-compromised
nude
mice
bearing
line
xenografts.
RESULTS
elevated
cells,
facilitating
enrichment
agents.
triggered
caspase-dependent
apoptosis
culture
if
at
high
doses,
while
pretreatment
potentiated
low
doses
suggested
these
synergistically
induced
lethality.
Consistent
vitro
data,
suppressed
human
xenografts
more
effectively
than
single
treatments
each
agent.
CONCLUSION
Our
findings
suggest
suppress
effectively.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(9), С. 4923 - 4923
Опубликована: Апрель 30, 2024
Treating
female
canine
mammary
gland
tumors
is
crucial
owing
to
their
propensity
for
rapid
progression
and
metastasis,
significantly
impacting
the
overall
health
well-being
of
dogs.
Mitoquinone
(MitoQ),
an
antioxidant,
has
shown
promise
in
inhibiting
migration,
invasion,
clonogenicity
human
breast
cancer
cells.
Thus,
we
investigated
MitoQ's
potential
anticancer
properties
against
tumor
cells,
CMT-U27
CF41.Mg.
MitoQ
markedly
suppressed
proliferation
migration
both
CF41.Mg
cells
induced
apoptotic
cell
death
a
dose-dependent
manner.
Furthermore,
treatment
with
led
increased
levels
pro-apoptotic
proteins,
including
cleaved-caspase3,
BAX,
phospho-p53.
Cell
cycle
analysis
revealed
that
hindered
G1
S
phases
These
findings
were
supported
using
western
blot
analysis,
demonstrating
elevated
cleaved
caspase-3,
hallmark
apoptosis,
decreased
expression
cyclin-dependent
kinase
(CDK)
2
cyclin
D4,
pivotal
regulators
cycle.
In
conclusion,
exhibits
vitro
antitumor
effects
by
inducing
apoptosis
arresting
tumors,
suggesting
its
as
preventive
or
therapeutic
agent
cancer.
Cancer & Metabolism,
Год журнала:
2024,
Номер
12(1)
Опубликована: Июль 8, 2024
Abstract
Background
Despite
technological
advances
in
radiotherapy,
cancer
cells
at
the
tumor
margin
and
diffusive
infiltrates
can
receive
subcytotoxic
doses
of
photons.
Even
if
only
a
minority
are
concerned,
phenotypic
consequences
could
be
important
considering
that
mitochondrial
DNA
(mtDNA)
is
primary
target
radiation
damage
to
mtDNA
persist.
In
turn,
dysfunction
associated
with
enhanced
ROS
(mtROS)
production
promote
cell
migration
out
irradiation
field
natural
attempt
escape
therapy.
this
study,
using
MCF7
MDA-MB-231
human
breast
as
models,
we
aimed
elucidate
molecular
mechanisms
supporting
contribution
induced
by
subclinical
(<
2
Gy).
Methods
Mitochondrial
was
tested
multiplex
PCR,
oximetry,
ROS-sensitive
fluorescent
reporters.
Migration
transwells
48
h
after
presence
or
absence
inhibitors
targeting
specific
downstream
effectors.
Among
inhibitors,
designed
mitochondria-targeted
version
catalase
(mtCAT)
selectively
inactivate
H
O
.
Results
Photon
(0.5
Gy
for
0.125
cells)
sequentially
affected
levels
and/or
integrity,
increased
mtROS
production,
MAP2K1/MEK1
gene
expression,
activated
transcription
factors
NF-κB
AP1
stimulated
migration.
Targeting
pharmacologically
MitoQ
genetically
mtCAT
expression
mitigated
dose
irradiation.
Conclusion
Subclinical
photon
migration,
which
countered
mtROS.
