FEBS Letters,
Journal Year:
2018,
Volume and Issue:
592(5), P. 793 - 811
Published: Jan. 24, 2018
The
mitochondrial
transcription
factor
A,
or
TFAM
,
is
a
DNA
(mt
)‐binding
protein
essential
for
genome
maintenance.
functions
in
determining
the
abundance
of
by
regulating
packaging,
stability,
and
replication.
More
recently,
has
been
shown
to
play
central
role
mt
stress‐mediated
inflammatory
response.
Emerging
evidence
indicates
that
decreased
copy
number
associated
with
several
aging‐related
pathologies;
however,
little
known
about
association
disease.
In
this
Review,
we
evaluate
potential
associations
altered
levels
neurodegeneration.
We
also
describe
mechanisms
which
replication,
initiation,
‐mediated
endogenous
danger
signals
may
impact
homeostasis
Alzheimer,
Huntington,
Parkinson,
other
neurodegenerative
diseases.
Cell Death and Differentiation,
Journal Year:
2018,
Volume and Issue:
25(3), P. 486 - 541
Published: Jan. 23, 2018
Over
the
past
decade,
Nomenclature
Committee
on
Cell
Death
(NCCD)
has
formulated
guidelines
for
definition
and
interpretation
of
cell
death
from
morphological,
biochemical,
functional
perspectives.
Since
field
continues
to
expand
novel
mechanisms
that
orchestrate
multiple
pathways
are
unveiled,
we
propose
an
updated
classification
subroutines
focusing
mechanistic
essential
(as
opposed
correlative
dispensable)
aspects
process.
As
provide
molecularly
oriented
definitions
terms
including
intrinsic
apoptosis,
extrinsic
mitochondrial
permeability
transition
(MPT)-driven
necrosis,
necroptosis,
ferroptosis,
pyroptosis,
parthanatos,
entotic
death,
NETotic
lysosome-dependent
autophagy-dependent
immunogenic
cellular
senescence,
mitotic
catastrophe,
discuss
utility
neologisms
refer
highly
specialized
instances
these
processes.
The
mission
NCCD
is
a
widely
accepted
nomenclature
in
support
continued
development
field.
Nature Communications,
Journal Year:
2020,
Volume and Issue:
11(1)
Published: Jan. 3, 2020
Abstract
Mitochondria
are
signaling
organelles
that
regulate
a
wide
variety
of
cellular
functions
and
can
dictate
cell
fate.
Multiple
mechanisms
contribute
to
communicate
mitochondrial
fitness
the
rest
cell.
Recent
evidence
confers
new
role
for
TCA
cycle
intermediates,
generally
thought
be
important
biosynthetic
purposes,
as
molecules
with
controlling
chromatin
modifications,
DNA
methylation,
hypoxic
response,
immunity.
This
review
summarizes
by
which
abundance
different
metabolites
controls
function
fate
in
contexts.
We
will
focus
on
how
these
mediated
affect
physiology
disease.
Science,
Journal Year:
2018,
Volume and Issue:
359(6378)
Published: Feb. 22, 2018
Mitochondrial
apoptosis
is
mediated
by
BAK
and
BAX,
two
proteins
that
induce
mitochondrial
outer
membrane
permeabilization,
leading
to
cytochrome
c
release
activation
of
apoptotic
caspases.
In
the
absence
active
caspases,
DNA
(mtDNA)
triggers
innate
immune
cGAS/STING
pathway,
causing
dying
cells
secrete
type
I
interferon.
How
cGAS
gains
access
mtDNA
remains
unclear.
We
used
live-cell
lattice
light-sheet
microscopy
examine
network
in
mouse
embryonic
fibroblasts.
found
after
BAK/BAX
loss,
broke
down
large
pores
appeared
membrane.
These
macropores
allowed
inner
herniate
into
cytosol,
carrying
with
it
matrix
components,
including
genome.
Apoptotic
caspases
did
not
prevent
herniation
but
dismantled
cell
suppress
mtDNA-induced
signaling.
Cell Death and Disease,
Journal Year:
2020,
Volume and Issue:
11(11)
Published: Nov. 26, 2020
Abstract
Chemotherapy,
radiation
therapy,
as
well
targeted
anticancer
agents
can
induce
clinically
relevant
tumor-targeting
immune
responses,
which
critically
rely
on
the
antigenicity
of
malignant
cells
and
their
capacity
to
generate
adjuvant
signals.
In
particular,
immunogenic
cell
death
(ICD)
is
accompanied
by
exposure
release
numerous
damage-associated
molecular
patterns
(DAMPs),
altogether
confer
a
robust
adjuvanticity
dying
cancer
cells,
they
favor
recruitment
activation
antigen-presenting
cells.
ICD-associated
DAMPs
include
surface-exposed
calreticulin
(CALR)
secreted
ATP,
annexin
A1
(ANXA1),
type
I
interferon,
high-mobility
group
box
1
(HMGB1).
Additional
hallmarks
ICD
encompass
phosphorylation
eukaryotic
translation
initiation
factor
2
subunit-α
(EIF2S1,
better
known
eIF2α),
autophagy,
global
arrest
in
transcription
translation.
Here,
we
outline
methodological
approaches
for
measuring
markers
vitro
ex
vivo
discovery
next-generation
antineoplastic
agents,
development
personalized
regimens,
identification
optimal
therapeutic
combinations
clinical
management
cancer.
Annual Review of Pathology Mechanisms of Disease,
Journal Year:
2019,
Volume and Issue:
15(1), P. 493 - 518
Published: Nov. 1, 2019
Recognizing
the
importance
of
leukocyte
trafficking
in
inflammation
led
to
some
therapeutic
breakthroughs.
However,
many
inflammatory
pathologies
remain
without
specific
therapy.
This
review
discusses
leukocytes
context
sterile
inflammation,
a
process
caused
by
(non-microbial)
molecules,
comprising
damage-associated
molecular
patterns
(DAMPs).
DAMPs
bind
receptors
activate
and
start
highly
optimized
sequence
immune
cell
recruitment
neutrophils
monocytes
initiate
effective
tissue
repair.
When
are
cleared,
recruited
change
from
proinflammatory
reparative
program,
switch
that
is
locally
supervised
invariant
natural
killer
T
cells.
In
addition,
exit
site
reverse
transmigrate
back
bloodstream.
Inflammation
persists
when
program
or
transmigration
fails,
coordinated
effort
cannot
clear
immunostimulatory
molecules.
The
latter
causes
inappropriate
activation,
driver
associated
with
poor
lifestyle
choices.
We
discuss
lifestyle-associated
diseases
their
corresponding
(LAMPs)
distinguish
them
DAMPs.
