Antioxidants,
Год журнала:
2025,
Номер
14(4), С. 372 - 372
Опубликована: Март 21, 2025
Mitochondria
are
of
great
importance
in
cell
biology
since
they
major
sites
adenosine
triphosphate
(ATP)
production
and
widely
involved
different
cellular
pathways
the
response
to
stress.
During
ATP
production,
reactive
oxygen
species
(ROS)
can
be
produced.
While
a
small
amount
ROS
may
important
for
regulation
physiological
processes,
at
elevated
levels
turn
into
harmful
agents
leading
damage.
From
pathological
perspective,
it
could
particularly
interesting
focus
on
mitochondrial
function
endothelial
cells
development
aging
onset
diseases,
including
renal,
cardio-metabolic,
liver
neurodegenerative
ones.
However,
date,
there
no
surveys
which
address
above
issues.
To
fill
this
gap,
valuable
collect
recent
findings
about
role
mitochondria
function,
not
only
increase
knowledge
but
also
clinical
applications.
Here,
we
overview
most
issues
view
characterizing
as
an
innovative
potential
target
prevention
aging,
well
treatment
conditions.
Frontiers in Endocrinology,
Год журнала:
2024,
Номер
15
Опубликована: Апрель 5, 2024
Diabetic
vascular
complications
are
prevalent
and
severe
among
diabetic
patients,
profoundly
affecting
both
their
quality
of
life
long-term
prospects.
These
can
be
classified
into
macrovascular
microvascular
complications.
Under
the
impact
risk
factors
such
as
elevated
blood
glucose,
pressure,
cholesterol
lipids,
endothelium
undergoes
endothelial
dysfunction,
characterized
by
increased
inflammation
oxidative
stress,
decreased
NO
biosynthesis,
endothelial-mesenchymal
transition,
senescence,
even
cell
death.
processes
will
ultimately
lead
to
diseases,
with
diseases
mainly
atherosclerosis
(AS)
thickening
basement
membrane.
It
further
indicates
a
primary
contributor
morbidity
mortality
observed
in
individuals
diabetes.
In
this
review,
we
delve
intricate
mechanisms
that
drive
dysfunction
during
diabetes
progression
its
associated
Furthermore,
outline
various
pharmacotherapies
targeting
hope
accelerating
effective
therapeutic
drug
discovery
for
early
control
Pharmacological Research,
Год журнала:
2024,
Номер
200, С. 107057 - 107057
Опубликована: Янв. 11, 2024
Mitochondria-associated
ferroptosis
exacerbates
cardiac
microvascular
dysfunction
in
diabetic
cardiomyopathy
(DCM).
Nicorandil,
an
ATP-sensitive
K+
channel
opener,
protects
against
endothelial
dysfunction,
mitochondrial
and
DCM;
however,
its
effects
on
mitophagy
remain
unexplored.
The
present
study
aimed
to
assess
the
beneficial
of
nicorandil
DCM
underlying
mechanisms.
Cardiac
perfusion
was
assessed
using
a
lectin
assay,
while
via
mt-Keima
transfection
transmission
electron
microscopy.
Ferroptosis
examined
mRNA
sequencing,
fluorescence
staining,
western
blotting.
localization
Parkin,
ACSL4,
AMPK
determined
immunofluorescence
staining.
Following
long-term
diabetes,
treatment
improved
function
remodeling
by
alleviating
injuries,
as
evidenced
structural
integrity.
mRNA-sequencing
biochemical
analyses
showed
that
occurred
Pink1/Parkin-dependent
suppressed
cells
after
diabetes.
Nicorandil
mitochondria-associated
promoting
mitophagy.
Moreover,
increased
phosphorylation
level
AMPKα1
promoted
translocation,
which
further
inhibited
translocation
ACSL4
ultimately
ferroptosis.
Importantly,
overexpression
mitochondria-localized
(mitoAα1)
shared
similar
benefits
with
mitophagy,
cardiovascular
protection
injury.
In
conclusion,
demonstrated
therapeutic
revealed
AMPK-Parkin-ACSL4
signaling
pathway
mediates
development
dysfunction.
International Journal of Biological Sciences,
Год журнала:
2024,
Номер
20(11), С. 4458 - 4475
Опубликована: Янв. 1, 2024
This
study
investigated
the
mechanism
by
which
NR4A1
regulates
mitochondrial
fission
factor
(Mff)-related
and
FUN14
domain
1
(FUNDC1)-mediated
mitophagy
following
cardiac
ischemia-reperfusion
injury(I/R).
Our
findings
showed
that
damage
regulation
was
positively
correlated
with
pathological
pan-apoptosis
of
myocardial
cell
mitochondria.
Compared
wild-type
mice
(WT),
NR4A1-knockout
exhibited
resistance
to
injury
fission,
characterized
activation.
Results
increased
expression
level,
activating
mediated
Mff
restoring
phenotype
FUNDC1.
The
inactivation
FUNDC1
phosphorylation
could
not
mediate
normalization
in
a
timely
manner,
leading
an
excessive
stress
response
unfolded
proteins
imbalance
homeostasis.
process
disrupted
quality
control
network,
accumulation
damaged
mitochondria
activation
pan-apoptotic
programs.
data
indicate
is
novel
critical
target
I/R
exertsand
negative
regulatory
effects
Mff-mediated
mito-fission
inhibiting
FUNDC1-mediated
mitophagy.
Targeting
crosstalk
balance
between
NR4A1-Mff-FUNDC1
potential
approach
for
treating
I/R.
Biomedicines,
Год журнала:
2022,
Номер
10(9), С. 2274 - 2274
Опубликована: Сен. 14, 2022
Diabetic
patients
are
frequently
affected
by
coronary
microvascular
dysfunction
(CMD),
a
condition
consisting
of
combination
altered
vasomotion
and
long-term
structural
change
to
arterioles
leading
impaired
regulation
blood
flow
in
response
changing
cardiomyocyte
oxygen
requirements.
The
pathogenesis
this
complication
is
complex
not
completely
known,
involving
several
alterations
among
which
hyperglycemia
insulin
resistance
play
particularly
central
roles
oxidative
stress,
inflammatory
activation
barrier
function
endothelium.
CMD
significantly
contributes
cardiac
events
such
as
angina
or
infarction
without
obstructive
artery
disease,
well
heart
failure,
especially
the
phenotype
associated
with
preserved
ejection
fraction,
greatly
impact
cardiovascular
(CV)
prognosis.
To
date,
no
treatments
specifically
target
vascular
damage,
but
recent
experimental
studies
some
clinical
investigations
have
produced
data
favor
potential
beneficial
effects
on
micro
vessels
caused
two
classes
glucose-lowering
drugs:
glucagon-like
peptide
1
(GLP-1)-based
therapy
inhibitors
sodium-glucose
cotransporter-2
(SGLT2).
purpose
review
describe
pathophysiological
mechanisms,
manifestations
particular
reference
diabetes,
summarize
protective
antidiabetic
drugs
myocardial
compartment.
Journal of Translational Medicine,
Год журнала:
2023,
Номер
21(1)
Опубликована: Июль 5, 2023
Endothelial
cells
(ECs)
angiogenesis
is
the
process
of
sprouting
new
vessels
from
existing
ones,
playing
critical
roles
in
physiological
and
pathological
processes
such
as
wound
healing,
placentation,
ischemia/reperfusion,
cardiovascular
diseases
cancer
metastasis.
Although
mitochondria
are
not
major
sites
energy
source
ECs,
they
function
important
biosynthetic
signaling
hubs
to
regulate
ECs
metabolism
adaptations
local
environment,
thus
affecting
migration,
proliferation
angiogenic
process.
The
understanding
importance
potential
mechanisms
regulating
metabolism,
has
developed
past
decades.
Thus,
this
review,
we
discuss
current
mitochondrial
proteins
molecules
angiogeneic
signaling,
provide
therapeutic
targets
for
treatment
diverse
angiogenesis-dependent
diseases.
Frontiers in Immunology,
Год журнала:
2023,
Номер
14
Опубликована: Май 16, 2023
Mitophagy
is
a
type
of
autophagy
that
can
selectively
eliminate
damaged
and
depolarized
mitochondria
to
maintain
mitochondrial
activity
cellular
homeostasis.
Several
pathways
have
been
found
participate
in
different
steps
mitophagy.
plays
significant
role
the
homeostasis
physiological
function
vascular
endothelial
cells,
smooth
muscle
macrophages,
involved
development
atherosclerosis
(AS).
At
present,
many
medications
natural
chemicals
shown
alter
mitophagy
slow
progression
AS.
This
review
serves
as
an
introduction
field
for
researchers
interested
targeting
this
pathway
part
potential
AS
management
strategy.
Biomedicine & Pharmacotherapy,
Год журнала:
2023,
Номер
159, С. 114171 - 114171
Опубликована: Янв. 13, 2023
Mitochondrial
dysfunction
is
the
main
cause
of
damage
to
pathological
mechanism
ischemic
cardiomyopathy.
In
addition,
mitochondrial
can
also
affect
homeostasis
cardiomyocytes
or
endothelial
cell
dysfunction,
leading
a
vicious
cycle
oxidative
stress.
And
an
important
basis
for
cardiomyopathy
and
reperfusion
injury
after
myocardial
infarction
end-stage
coronary
heart
disease.
Therefore,
mitochondria
be
used
as
therapeutic
targets
against
ischemia
injury,
regulation
morphology,
function
structure
key
way
targeting
quality
control
mechanisms.
includes
mechanisms
such
mitophagy,
dynamics
(mitochondrial
fusion/fission),
biosynthesis,
unfolded
protein
responses.
Among
them,
increase
fragmentation
caused
by
fission
initial
factor.
The
protective
fusion
strengthen
interaction
synthesis
paired
promote
biosynthesis.
hypoxia,
formation
fragments,
fragmented
lead
damaged
DNA
production,
which
biosynthesis
insufficient
ATP
ROS.
Burst
growth
loss
membrane
potential.
This
eventually
leads
accumulation
mitochondria.
Then,
under
leadership
complete
degradation
process
through
transport
morphologically
structurally
lysosomes
degradation.
But
once
increases,
may
activate
pathway
cardiomyocyte
death.
Although
laboratory
studies
have
found
that
variety
mitochondrial-targeted
drugs
reduce
protect
cardiomyocytes,
there
are
still
few
successfully
passed
clinical
trials.
this
review,
we
describe
role
MQS
in
ischemia/hypoxia-induced
physiopathology
elucidate
relevant
further
explained
advantages
natural
products
improving
protecting
cells
from
perspective
pharmacological
mechanism,
its
related
Potential
targeted
therapies
improve
ischemia/hypoxia
discussed,
aiming
accelerate
development
cardioprotective
dysfunction.
