Journal of Advanced Research,
Год журнала:
2024,
Номер
65, С. 297 - 327
Опубликована: Май 14, 2024
Autophagy
is
an
evolutionarily
conserved
turnover
process
for
intracellular
substances
in
eukaryotes,
relying
on
lysosomal
(in
animals)
or
vacuolar
yeast
and
plants)
mechanisms.
In
the
past
two
decades,
emerging
evidence
suggests
that,
under
specific
conditions,
autophagy
can
target
particular
macromolecules
organelles
degradation,
a
termed
selective
autophagy.
Recently,
accumulating
studies
have
demonstrated
that
abnormality
of
closely
associated
with
occurrence
progression
many
human
diseases,
including
neurodegenerative
cancers,
metabolic
cardiovascular
diseases.
This
review
aims
at
systematically
comprehensively
introducing
its
role
various
while
unravelling
molecular
mechanisms
By
providing
theoretical
basis
development
related
small-molecule
drugs
as
well
treating
this
seeks
to
contribute
understanding
therapeutic
potential.
review,
we
introduce
dissect
major
categories
been
discovered.
We
also
focus
recent
advances
underlying
both
classical
non-classical
Moreover,
current
situation
targeting
different
types
further
summarized,
valuable
insights
into
discovery
more
candidate
future.
On
other
hand,
reveal
clinically
relevant
implementations
are
potentially
autophagy,
such
predictive
approaches
treatments
tailored
individual
patients.
International Journal of Molecular Sciences,
Год журнала:
2022,
Номер
23(6), С. 3025 - 3025
Опубликована: Март 11, 2022
Mitochondria
are
the
sites
of
oxidative
metabolism
in
eukaryotes
where
metabolites
sugars,
fats,
and
amino
acids
oxidized
to
harvest
energy.
Notably,
mitochondria
store
Ca2+
work
synergy
with
organelles
such
as
endoplasmic
reticulum
extracellular
matrix
control
dynamic
balance
concentration
cells.
vital
heart
tissue.
Mitochondrial
homeostasis
is
particularly
important
for
maintaining
physiological
pathological
mechanisms
heart.
plays
a
key
role
regulation
cardiac
energy
metabolism,
death,
oxygen
free
radical
production,
autophagy.
The
imbalance
mitochondrial
closely
associated
remodeling.
uniporter
(mtCU)
protein
complex
responsible
uptake
release
consequently,
This
review
summarizes
remodeling
regulatory
effects
calcium
on
cell
autophagy,
also
provides
theoretical
basis
novel
target
treatment
cardiovascular
diseases.
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.
Experimental & Molecular Medicine,
Год журнала:
2023,
Номер
55(1), С. 269 - 280
Опубликована: Янв. 19, 2023
Abstract
Mitochondrial
DNA
(mtDNA)
released
through
protein
oligomers,
such
as
voltage-dependent
anion
channel
1
(VDAC1),
triggers
innate
immune
activation
and
thus
contributes
to
liver
fibrosis.
Here,
we
investigated
the
role
of
Parkin,
an
important
regulator
mitochondria,
its
regulation
VDAC1-mediated
mtDNA
release
in
The
circulating
mitochondrial
levels
Parkin
VDAC1
were
upregulated
patients
with
A
4-week
CCl
4
challenge
induced
mtDNA,
STING
signaling,
a
decline
autophagy,
apoptosis
mouse
livers,
knockout
aggravated
these
effects.
In
addition,
reduced
prevented
oligomerization
manner
dependent
on
E3
activity
hepatocytes.
We
found
that
site-specific
ubiquitination
at
lysine
53
by
interrupted
into
cytoplasm
under
stress.
ubiquitination-defective
K53R
mutant
predominantly
formed
oligomers
resisted
suppression
Parkin.
Hepatocytes
expressing
exhibited
activated
signaling
pathway
hepatic
stellate
cells,
this
effect
could
not
be
abolished
propose
specific
site
confers
protection
against
fibrosis
interrupting
release.
Frontiers in Cell and Developmental Biology,
Год журнала:
2023,
Номер
11
Опубликована: Ноя. 6, 2023
Cardiovascular
diseases
(CVDs)
are
one
of
the
primary
causes
mortality
worldwide.
An
optimal
mitochondrial
function
is
central
to
supplying
tissues
with
high
energy
demand,
such
as
cardiovascular
system.
In
addition
producing
ATP
a
power
source,
mitochondria
also
heavily
involved
in
adaptation
environmental
stress
and
fine-tuning
tissue
functions.
Mitochondrial
quality
control
(MQC)
through
fission,
fusion,
mitophagy,
biogenesis
ensures
clearance
dysfunctional
preserves
homeostasis
tissues.
Furthermore,
generate
reactive
oxygen
species
(ROS),
which
trigger
production
pro-inflammatory
cytokines
regulate
cell
survival.
dysfunction
has
been
implicated
multiple
CVDs,
including
ischemia-reperfusion
(I/R),
atherosclerosis,
heart
failure,
cardiac
hypertrophy,
hypertension,
diabetic
genetic
cardiomyopathies,
Kawasaki
Disease
(KD).
Thus,
MQC
pivotal
promoting
health.
Here,
we
outline
mechanisms
discuss
current
literature
on
CVDs.
Journal of Advanced Research,
Год журнала:
2024,
Номер
65, С. 297 - 327
Опубликована: Май 14, 2024
Autophagy
is
an
evolutionarily
conserved
turnover
process
for
intracellular
substances
in
eukaryotes,
relying
on
lysosomal
(in
animals)
or
vacuolar
yeast
and
plants)
mechanisms.
In
the
past
two
decades,
emerging
evidence
suggests
that,
under
specific
conditions,
autophagy
can
target
particular
macromolecules
organelles
degradation,
a
termed
selective
autophagy.
Recently,
accumulating
studies
have
demonstrated
that
abnormality
of
closely
associated
with
occurrence
progression
many
human
diseases,
including
neurodegenerative
cancers,
metabolic
cardiovascular
diseases.
This
review
aims
at
systematically
comprehensively
introducing
its
role
various
while
unravelling
molecular
mechanisms
By
providing
theoretical
basis
development
related
small-molecule
drugs
as
well
treating
this
seeks
to
contribute
understanding
therapeutic
potential.
review,
we
introduce
dissect
major
categories
been
discovered.
We
also
focus
recent
advances
underlying
both
classical
non-classical
Moreover,
current
situation
targeting
different
types
further
summarized,
valuable
insights
into
discovery
more
candidate
future.
On
other
hand,
reveal
clinically
relevant
implementations
are
potentially
autophagy,
such
predictive
approaches
treatments
tailored
individual
patients.
