Antioxidants,
Год журнала:
2018,
Номер
7(1), С. 13 - 13
Опубликована: Янв. 16, 2018
Mitochondria
are
organelles
with
a
highly
dynamic
ultrastructure
maintained
by
delicate
equilibrium
between
its
fission
and
fusion
rates.
Understanding
the
factors
influencing
this
balance
is
important
as
perturbations
to
mitochondrial
dynamics
can
result
in
pathological
states.
As
terminal
site
of
nutrient
oxidation
for
cell,
powerhouses
harness
energy
form
ATP
process
driven
electron
transport
chain.
Contemporaneously,
electrons
translocated
within
chain
undergo
spontaneous
side
reactions
oxygen,
giving
rise
superoxide
variety
other
downstream
reactive
oxygen
species
(ROS).
Mitochondrially-derived
ROS
mediate
redox
signaling
or,
excess,
cause
cell
injury
even
death.
Recent
evidence
suggests
that
tightly
coupled
generation
depending
on
physiological
status
cell.
Yet,
mechanism
which
changes
shape
modulate
function
homeostasis
less
clear.
Aberrant
morphology
may
lead
enhanced
formation,
which,
turn,
deteriorate
health
further
exacerbate
oxidative
stress
self-perpetuating
vicious
cycle.
Here,
we
review
latest
findings
intricate
relationship
production,
focusing
mainly
role
malignant
disease.
Redox Biology,
Год журнала:
2017,
Номер
15, С. 335 - 346
Опубликована: Дек. 30, 2017
Impaired
cardiac
microvascular
function
contributes
to
diabetic
cardiovascular
complications
although
effective
therapy
remains
elusive.
Empagliflozin,
a
sodium-glucose
cotransporter
2
(SGLT2)
inhibitor
recently
approved
for
treatment
of
type
diabetes,
promotes
glycosuria
excretion
and
offers
cardioprotective
actions
beyond
its
glucose-lowering
effects.
This
study
was
designed
evaluate
the
effect
empagliflozin
on
injury
in
diabetes
underlying
mechanism
involved
with
focus
mitochondria.
Our
data
revealed
that
improved
myocardial
structure
function,
preserved
barrier
integrity,
sustained
eNOS
phosphorylation
endothelium-dependent
relaxation,
as
well
microvessel
density
perfusion.
Further
suggested
exerted
effects
through
inhibition
mitochondrial
fission
an
adenosine
monophosphate
(AMP)-activated
protein
kinase
(AMPK)-dependent
manner.
Empagliflozin
restored
AMP-to-ATP
ratio
trigger
AMPK
activation,
suppressed
Drp1S616
phosphorylation,
increased
Drp1S637
ultimately
leading
fission.
The
empagliflozin-induced
endothelial
cell
(CMEC)
reactive
oxygen
species
(mtROS)
production
subsequently
oxidative
stress
impede
CMEC
senescence.
Empagliflozin-induced
loss
also
favored
angiogenesis
by
promoting
migration
amelioration
F-actin
depolymerization.
Taken
together,
these
results
indicated
therapeutic
promises
pathological
changes
diabetes.
Cell Reports,
Год журнала:
2017,
Номер
21(1), С. 1 - 9
Опубликована: Окт. 1, 2017
Reactive
oxygen
species
(ROS)
are
continuously
produced
as
a
by-product
of
mitochondrial
metabolism
and
eliminated
via
antioxidant
systems.
Regulation
mitochondrially
ROS
is
required
for
proper
cellular
function,
adaptation
to
metabolic
stress,
bypassing
senescence.
Here,
we
report
non-canonical
regulation
the
energy
sensor
AMP-activated
protein
kinase
(AMPK)
by
(mROS)
that
functions
maintain
homeostasis.
We
demonstrate
physiological
activator
AMPK
activation
triggers
PGC-1α-dependent
response
limits
production.
Cells
lacking
activity
display
increased
levels
undergo
premature
Finally,
show
AMPK-PGC-1α-dependent
control
regulates
HIF-1α
stabilization
promote
Warburg
effect
in
cells
signaling.
These
data
highlight
key
function
sensing
resolving
stress
resistance
maintaining
balance.
Frontiers in Cell and Developmental Biology,
Год журнала:
2020,
Номер
8
Опубликована: Июнь 24, 2020
Mitochondria
are
highly
plastic
and
dynamic
organelles
that
have
graded
responses
to
the
changing
cellular,
environmental
developmental
cues.
undergo
constant
mitochondrial
fission
fusion,
biogenesis
mitophagy,
which
coordinately
control
morphology,
quantity,
quality,
turnover
inheritance.
Mitophagy
is
a
cellular
process
selectively
removes
aged
damaged
mitochondria
via
specific
sequestration
engulfment
of
for
subsequent
lysosomal
degradation.
It
plays
pivotal
role
reinstate
homeostasis
in
normal
physiology
conditions
stress.
Damaged
may
either
instigate
innate
immunity
through
overproduction
ROS
or
release
mtDNA,
trigger
cell
death
cytochrome
c
other
apoptogenic
factors
when
damage
beyond
repair.
Distinct
molecular
machineries
signaling
pathways
found
regulate
these
dynamics
behaviors.
less
clear
how
behaviors
coordinated
at
levels.
BCL2
family
proteins
interact
within
members
outer
membrane
permeabilization
apoptosis.
They
were
also
described
as
global
regulators
fate
their
interaction
with
distinct
partners
including
Drp1,
mitofusins,
PGAM5
even
LC3
involved
In
this
review,
we
summarize
recent
findings
on
governing
mitophagy
its
coordination
behaviors,
together
determine
fate.
Antioxidants,
Год журнала:
2018,
Номер
7(1), С. 13 - 13
Опубликована: Янв. 16, 2018
Mitochondria
are
organelles
with
a
highly
dynamic
ultrastructure
maintained
by
delicate
equilibrium
between
its
fission
and
fusion
rates.
Understanding
the
factors
influencing
this
balance
is
important
as
perturbations
to
mitochondrial
dynamics
can
result
in
pathological
states.
As
terminal
site
of
nutrient
oxidation
for
cell,
powerhouses
harness
energy
form
ATP
process
driven
electron
transport
chain.
Contemporaneously,
electrons
translocated
within
chain
undergo
spontaneous
side
reactions
oxygen,
giving
rise
superoxide
variety
other
downstream
reactive
oxygen
species
(ROS).
Mitochondrially-derived
ROS
mediate
redox
signaling
or,
excess,
cause
cell
injury
even
death.
Recent
evidence
suggests
that
tightly
coupled
generation
depending
on
physiological
status
cell.
Yet,
mechanism
which
changes
shape
modulate
function
homeostasis
less
clear.
Aberrant
morphology
may
lead
enhanced
formation,
which,
turn,
deteriorate
health
further
exacerbate
oxidative
stress
self-perpetuating
vicious
cycle.
Here,
we
review
latest
findings
intricate
relationship
production,
focusing
mainly
role
malignant
disease.
