Science,
Journal Year:
2011,
Volume and Issue:
333(6046), P. 1109 - 1112
Published: Aug. 25, 2011
Alterations
of
mitochondrial
functions
are
linked
to
multiple
degenerative
or
acute
diseases.
As
mitochondria
age
in
our
cells,
they
become
progressively
inefficient
and
potentially
toxic,
damage
can
trigger
the
permeabilization
membranes
initiate
apoptosis
necrosis.
Moreover,
have
an
important
role
pro-inflammatory
signaling.
Autophagic
turnover
cellular
constituents,
be
it
general
specific
for
(mitophagy),
eliminates
dysfunctional
damaged
mitochondria,
thus
counteracting
degeneration,
dampening
inflammation,
preventing
unwarranted
cell
loss.
Decreased
expression
genes
that
regulate
autophagy
mitophagy
cause
diseases
which
deficient
quality
control
results
inflammation
death
populations.
Thus,
a
combination
dysfunction
insufficient
may
contribute
aging-associated
pathologies.
Cell Death and Differentiation,
Journal Year:
2014,
Volume and Issue:
22(3), P. 377 - 388
Published: Sept. 26, 2014
Autophagy
is
a
catabolic
process
aimed
at
recycling
cellular
components
and
damaged
organelles
in
response
to
diverse
conditions
of
stress,
such
as
nutrient
deprivation,
viral
infection
genotoxic
stress.
A
growing
amount
evidence
recent
years
argues
for
oxidative
stress
acting
the
converging
point
these
stimuli,
with
reactive
oxygen
species
(ROS)
nitrogen
(RNS)
being
among
main
intracellular
signal
transducers
sustaining
autophagy.
This
review
aims
providing
novel
insight
into
regulatory
pathways
autophagy
glucose
amino
acid
well
their
tight
interconnection
metabolic
networks
redox
homeostasis.
The
role
nitrosative
also
discussed
light
its
harmful
both
biomolecules
mediator
through
reversible
posttranslational
modifications
thiol-containing
proteins.
redox-independent
relationship
between
antioxidant
response,
occurring
p62/Keap1/Nrf2
pathway,
addressed
order
provide
wide
perspective
upon
Herein,
we
attempt
afford
an
overview
complex
crosstalk
DNA
damage
(DDR),
focusing
on
activated
ROS
RNS
overproduction.
Along
lines,
direct
indirect
DDR
dissected
depth.
Autophagy,
Journal Year:
2016,
Volume and Issue:
12(8), P. 1425 - 1428
Published: June 1, 2016
Macroautophagy/autophagy
is
an
evolutionarily
conserved
degradation
pathway
that
maintains
homeostasis.
Ferroptosis,
a
novel
form
of
regulated
cell
death,
characterized
by
production
reactive
oxygen
species
from
accumulated
iron
and
lipid
peroxidation.
However,
the
relationship
between
autophagy
ferroptosis
at
genetic
level
remains
unclear.
Here,
we
demonstrated
contributes
to
ferritin
in
fibroblasts
cancer
cells.
Knockout
or
knockdown
Atg5
(autophagy-related
5)
Atg7
limited
erastin-induced
with
decreased
intracellular
ferrous
levels,
Remarkably,
NCOA4
(nuclear
receptor
coactivator
4)
was
selective
cargo
for
autophagic
turnover
(namely
ferritinophagy)
ferroptosis.
Consistently,
inhibition
inhibited
suppressed
In
contrast,
overexpression
increased
promoted
These
findings
provide
insight
into
interplay
death.
New England Journal of Medicine,
Journal Year:
2011,
Volume and Issue:
365(6), P. 506 - 517
Published: June 30, 2011
Controversy
exists
about
the
timing
of
initiation
parenteral
nutrition
in
critically
ill
adults
whom
caloric
targets
cannot
be
met
by
enteral
alone.In
this
randomized,
multicenter
trial,
we
compared
early
(European
guidelines)
with
late
(American
and
Canadian
intensive
care
unit
(ICU)
to
supplement
insufficient
nutrition.
In
2312
patients,
was
initiated
within
48
hours
after
ICU
admission
(early-initiation
group),
whereas
2328
not
before
day
8
(late-initiation
group).
A
protocol
for
applied
both
groups,
insulin
infused
achieve
normoglycemia.Patients
late-initiation
group
had
a
relative
increase
6.3%
likelihood
being
discharged
alive
earlier
from
(hazard
ratio,
1.06;
95%
confidence
interval
[CI],
1.00
1.13;
P=0.04)
hospital
CI,
P=0.04),
without
evidence
decreased
functional
status
at
discharge.
Rates
death
rates
survival
90
days
were
similar
two
groups.
Patients
group,
as
early-initiation
fewer
infections
(22.8%
vs.
26.2%,
P=0.008)
lower
incidence
cholestasis
(P<0.001).
The
reduction
9.7%
proportion
patients
requiring
more
than
2
mechanical
ventilation
(P=0.006),
median
3
duration
renal-replacement
therapy
(P=0.008),
mean
health
costs
€1,110
(about
$1,600)
(P=0.04).Late
associated
faster
recovery
complications,
initiation.
(Funded
Methusalem
program
Flemish
government
others;
EPaNIC
ClinicalTrials.gov
number,
NCT00512122.).
Biochemical Journal,
Journal Year:
2011,
Volume and Issue:
441(2), P. 523 - 540
Published: Dec. 21, 2011
Reactive
oxygen
and
nitrogen
species
change
cellular
responses
through
diverse
mechanisms
that
are
now
being
defined.
At
low
levels,
they
signalling
molecules,
at
high
damage
organelles,
particularly
the
mitochondria.
Oxidative
associated
mitochondrial
dysfunction
may
result
in
energy
depletion,
accumulation
of
cytotoxic
mediators
cell
death.
Understanding
interface
between
stress
adaptation
death
then
is
important
for
understanding
redox
biology
disease
pathogenesis.
Recent
studies
have
found
one
major
sensor
this
switch
autophagy.
Autophagic
activities
mediated
by
a
complex
molecular
machinery
including
more
than
30
Atg
(AuTophaGy-related)
proteins
50
lysosomal
hydrolases.
Autophagosomes
form
membrane
structures,
sequester
damaged,
oxidized
or
dysfunctional
intracellular
components
direct
them
to
lysosomes
degradation.
This
autophagic
process
sole
known
mechanism
turnover.
It
has
been
speculated
autophagy
abnormal
function
oxidative
nitrative
stress.
Emerging
investigations
provided
new
how
mitochondria
(also
as
mitophagy)
controlled,
impact
on
The
present
review
highlights
recent
regulation
autophagy,
context
basic
mitophagy.
Furthermore,
we
discuss
reactive
species.
relevant
degenerative
diseases
which
occurs
over
time,
both
pathways
play
role.
Molecular and Cellular Biology,
Journal Year:
2011,
Volume and Issue:
32(1), P. 2 - 11
Published: Oct. 25, 2011
Living
cells
are
adaptive
self-sustaining
systems.
They
strictly
depend
on
the
sufficient
supply
of
oxygen,
energy,
and
nutrients
from
outside
in
order
to
sustain
their
internal
organization.
However,
as
autonomous
entities
they
able
monitor
appropriately
adapt
any
critical
fluctuation
environment.
In
case
insufficient
external
nutrient
or
augmented
energy
demands,
start
extensively
digest
own
interior.
This
process,
known
macroautophagy,
comprises
transport
cytosolic
portions
entire
organelles
lysosomal
compartment
via
specific
double-membrane
vesicles,
called
autophagosomes.
Although
upregulated
under
restriction,
a
low
level
basal
autophagy
is
likewise
crucial
cellular
homeostasis.
On
other
hand,
have
avoid
excessive
enduring
self-digestion.
The
delicate
balance
between
production
consumption
demanding
task.
complex
protein
network
that
senses
precisely
reacts
environmental
changes
thus
mainly
regulated
by
rapid
reversible
posttranslational
modifications
such
phosphorylation.
review
focuses
serine/threonine
kinases
AMP-activated
kinase,
mammalian
target
rapamycin
(mTOR),
unc-51-like
kinase
1/2
(Ulk1/2),
three
interconnected
major
junctions
within
regulating
signaling
network.