Pharmacology & Therapeutics,
Journal Year:
2024,
Volume and Issue:
259, P. 108666 - 108666
Published: May 17, 2024
Acute
myocardial
infarction
(AMI)
remains
a
leading
cause
of
death
worldwide.
Increased
formation
reactive
oxygen
species
(ROS)
during
the
early
reperfusion
phase
is
thought
to
trigger
lipid
peroxidation
and
disrupt
redox
homeostasis,
injury.
Whilst
mitochondrial
enzyme
aldehyde
dehydrogenase
2
(ALDH2)
chiefly
recognised
for
its
central
role
in
ethanol
metabolism,
substantial
experimental
evidence
suggests
an
additional
cardioprotective
ALDH2
independent
alcohol
intake,
which
mitigates
injury
by
detoxifying
breakdown
products
including
aldehydes,
malondialdehyde
(MDA)
4-hydroxynonenal
(4-HNE).
Epidemiological
that
mutant
variant
with
reduced
activity
highly
prevalent
East
Asian
population
increases
AMI
risk.
Additional
studies
have
uncovered
strong
association
between
coronary
heart
disease
this
variant.
It
appears
polymorphism
(in
particular,
ALDH2*2/2
carriers)
has
potential
wide-ranging
effects
on
thiol
reactivity,
tone
therefore
numerous
redox-related
signaling
processes,
resilience
cope
lifestyle-related
environmental
stressors,
ability
whole
body
achieve
balance.
In
review,
we
summarize
journey
from
reductase
linked
via
pre-clinical
aimed
at
stimulating
reduce
clinical
protective
heart.
Cells,
Journal Year:
2020,
Volume and Issue:
9(1), P. 222 - 222
Published: Jan. 16, 2020
Elucidation
of
the
mitochondrial
regulatory
mechanisms
for
understanding
muscle
bioenergetics
and
role
mitochondria
is
a
fundamental
problem
in
cellular
physiology
pathophysiology.
The
cytoskeleton
(microtubules,
intermediate
filaments,
microfilaments)
plays
central
maintenance
shape,
location,
motility.
In
addition,
numerous
interactions
between
cytoskeletal
proteins
can
actively
participate
regulation
respiration
oxidative
phosphorylation.
cardiac
skeletal
muscles,
positions
are
tightly
fixed,
providing
their
regular
arrangement
with
other
structures
such
as
sarcoplasmic
reticulum
cytoskeleton.
This
involve
association
voltage-dependent
anion
channel
(VDAC),
thereby,
governing
permeability
outer
membrane
(OMM)
to
metabolites,
regulating
cell
energy
metabolism.
Cardiomyocytes
myocardial
fibers
demonstrate
tubulin
beta-II
isoform
entirely
co-localized
mitochondria,
contrast
isoforms
tubulin.
observation
suggests
participation
OMM
through
interaction
VDAC.
also
regulated
by
specific
cytolinker
protein
plectin.
review
summarizes
discusses
previous
studies
on
metabolism
function,
adenosine
triphosphate
(ATP)
production,
transfer.
Bioactive Materials,
Journal Year:
2021,
Volume and Issue:
6(7), P. 2058 - 2069
Published: Jan. 12, 2021
Mitochondrial
damage
is
a
critical
driver
in
myocardial
ischemia-reperfusion
(I/R)
injury
and
can
be
alleviated
via
the
mitochondrial
transplantation.
The
efficiency
of
transplantation
determined
by
vitality.
Because
aldehyde
dehydrogenase
2
(ALDH2)
has
key
role
regulating
homeostasis,
we
aimed
to
investigate
its
potential
therapeutic
effects
on
use
ALDH2
activator,
Alda-1.
Our
present
study
demonstrated
that
time-dependent
internalization
exogenous
mitochondria
cardiomyocytes
along
with
ATP
production
were
significantly
increased
response
Furthermore,
Alda-1
treatment
remarkably
promoted
oxygen
consumption
rate
baseline
mechanical
function
caused
inhibited
cardiomyocyte
apoptosis
induced
hypoxia-reoxygenation
exposure,
independent
treatment.
However,
promotion
exposed
was
only
observed
after
By
using
I/R
mouse
model,
our
results
revealed
Alda-1-treated
into
tissues
limited
infarction
size
injury,
which
at
least
part
due
potential-mediated
fusion.
In
conclusion,
activation
shows
great
for
injury.
Cardiometry,
Journal Year:
2021,
Volume and Issue:
18, P. 121 - 130
Published: May 18, 2021
The
aim
is
to
study
some
mechanisms
of
regulation
apoptosis
and
self-organization
in
the
mitochondria
heart
cells
female
mice
during
growth
experimental
melanoma
B16/
F10
linked
with
chronic
neurogenic
pain
as
comorbid
pathology.
Cell Death Discovery,
Journal Year:
2023,
Volume and Issue:
9(1)
Published: Feb. 25, 2023
Understanding
the
complex
pathogenesis
in
myocardial
ischemia/reperfusion
(I/R)
injury
(IRI)
is
an
urgent
problem
clinical
trials.
Increasing
pieces
of
evidence
have
suggested
that
miRNAs
are
involved
occurrence
and
development
heart
diseases
by
regulating
mitochondria-related
gene
expression.
Mitochondria
been
acknowledged
as
key
triggers
cardiac
I/R
injury.
However,
potential
impact
miR-130a
on
mitochondria
remains
unclear
IRI.
Exploring
regulatory
mechanism
may
provide
a
new
target
for
IRI
therapy.
In
present
study,
we
found
significantly
increased
acute
infarction
(AMI)
patients
rats.
MiR-130a
could
downregulate
viability
cardiomyocytes
knockdown
protect
under
hypoxia-reoxygenation
(HR).
Over-expression
resulted
mitochondrial
dysfunction.
It
was
evidenced
decreases
ATP
production,
membrane
(MMP),
increase
reactive
oxygen
species
(ROS)
production.
suppression
against
damage,
show
elevation
production
rate
MMP,
reduce
ROS
We
further
explored
effect
quality
control
(QMC)
system
determining
mitochondrial-protein-specific
proteases
analyzed
morphology
fluorescence
imaging
electron
microscopy,
respectively.
noted
suppress
fusion
FUNDC1-mediated
mitophagy
to
accelerate
Moreover,
investigated
targeted
genes
understand
setting
revealed
GJA1,
GJA1
rescued
enhancing
oxidative
phosphorylation,
meanwhile
protecting
cell
viability,
activating
mitophagy.
addition,
activated
mitophagy,
while
reversed
relevant
response.
Collectively,
our
findings
suggest
regulates
targeting
Pharmacology & Therapeutics,
Journal Year:
2024,
Volume and Issue:
259, P. 108666 - 108666
Published: May 17, 2024
Acute
myocardial
infarction
(AMI)
remains
a
leading
cause
of
death
worldwide.
Increased
formation
reactive
oxygen
species
(ROS)
during
the
early
reperfusion
phase
is
thought
to
trigger
lipid
peroxidation
and
disrupt
redox
homeostasis,
injury.
Whilst
mitochondrial
enzyme
aldehyde
dehydrogenase
2
(ALDH2)
chiefly
recognised
for
its
central
role
in
ethanol
metabolism,
substantial
experimental
evidence
suggests
an
additional
cardioprotective
ALDH2
independent
alcohol
intake,
which
mitigates
injury
by
detoxifying
breakdown
products
including
aldehydes,
malondialdehyde
(MDA)
4-hydroxynonenal
(4-HNE).
Epidemiological
that
mutant
variant
with
reduced
activity
highly
prevalent
East
Asian
population
increases
AMI
risk.
Additional
studies
have
uncovered
strong
association
between
coronary
heart
disease
this
variant.
It
appears
polymorphism
(in
particular,
ALDH2*2/2
carriers)
has
potential
wide-ranging
effects
on
thiol
reactivity,
tone
therefore
numerous
redox-related
signaling
processes,
resilience
cope
lifestyle-related
environmental
stressors,
ability
whole
body
achieve
balance.
In
review,
we
summarize
journey
from
reductase
linked
via
pre-clinical
aimed
at
stimulating
reduce
clinical
protective
heart.
