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.
Physiological Reviews,
Journal Year:
2012,
Volume and Issue:
92(2), P. 689 - 737
Published: April 1, 2012
The
mammalian
stress-activated
families
of
mitogen-activated
protein
kinases
(MAPKs)
were
first
elucidated
in
1994,
and
by
2001,
substantial
progress
had
been
made
identifying
the
architecture
pathways
upstream
these
as
well
cataloguing
candidate
substrates.
This
information
remains
largely
sound.
Nevertheless,
an
informed
understanding
physiological
pathophysiological
roles
remained
to
be
accomplished.
In
past
decade,
there
has
explosion
new
work
using
RNAi
cells,
transgenic,
knockout
conditional
technology
mice
that
provided
valuable
insight
into
functions
MAPK
pathways.
These
findings
have
important
implications
our
organ
development,
innate
acquired
immunity,
diseases
such
atherosclerosis,
tumorigenesis,
type
2
diabetes.
developments
bring
us
within
striking
distance
development
validation
novel
treatment
strategies.
Herein
we
summarize
molecular
components
stress-regulated
their
regulation
described
thus
far.
We
then
review
some
vivo
Molecular Cancer,
Journal Year:
2020,
Volume and Issue:
19(1)
Published: Jan. 22, 2020
Abstract
Autophagy,
as
a
type
II
programmed
cell
death,
plays
crucial
roles
with
autophagy-related
(ATG)
proteins
in
cancer.
Up
to
now,
the
dual
role
of
autophagy
both
cancer
progression
and
inhibition
remains
controversial,
which
numerous
ATG
their
core
complexes
including
ULK1/2
kinase
complex,
autophagy-specific
class
III
PI3K
ATG9A
trafficking
system,
ATG12
LC3
ubiquitin-like
conjugation
systems,
give
multiple
activities
pathway
are
involved
initiation,
nucleation,
elongation,
maturation,
fusion
degradation.
Autophagy
dynamic
tumor-suppressive
or
tumor-promoting
different
contexts
stages
development.
In
early
tumorigenesis,
autophagy,
survival
quality-control
mechanism,
prevents
tumor
initiation
suppresses
progression.
Once
tumors
progress
late
stage
established
subjected
environmental
stresses,
degradation
recycling
contributes
growth
promotes
aggressiveness
cancers
by
facilitating
metastasis.
This
indicates
that
regulation
can
be
used
effective
interventional
strategies
for
therapy.
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.
