Immunity,
Journal Year:
2019,
Volume and Issue:
51(1), P. 77 - 89.e6
Published: June 19, 2019
Highlights•Tissue-resident,
SFB-elicited
Th17
cells
are
non-inflammatory•Citrobacter-elicited
show
high
plasticity
towards
inflammatory
cytokines•SFB
metabolically
similar
to
resting
memory
cells•Citrobacter
highly
glycolytic
effector
cellsSummaryT
helper
17
(Th17)
pathogenic
in
many
diseases,
but
also
support
the
integrity
of
intestinal
barrier
a
non-inflammatory
manner.
It
is
unclear
what
distinguishes
elicited
by
pathogens
and
tissue-resident
homeostatic
commensals.
Here,
we
compared
characteristics
differentiating
response
commensal
bacteria
(SFB)
those
pathogen
(Citrobacter
rodentium).
Homeostatic
exhibited
little
expression
cytokines,
were
characterized
metabolism
typical
quiescent
or
T
cells,
did
not
participate
processes.
In
contrast,
infection-induced
showed
extensive
pro-inflammatory
disseminated
widely
into
periphery,
engaged
aerobic
glycolysis
addition
oxidative
phosphorylation
for
cells.
These
findings
will
help
ensure
that
future
therapies
directed
against
do
inadvertently
damage
resident
gut
population.Graphical
abstract
Essays in Biochemistry,
Journal Year:
2018,
Volume and Issue:
62(3), P. 341 - 360
Published: July 20, 2018
Mitochondria
are
highly
dynamic
organelles
undergoing
coordinated
cycles
of
fission
and
fusion,
referred
as
‘mitochondrial
dynamics’,
in
order
to
maintain
their
shape,
distribution
size.
Their
transient
rapid
morphological
adaptations
crucial
for
many
cellular
processes
such
cell
cycle,
immunity,
apoptosis
mitochondrial
quality
control.
Mutations
the
core
machinery
components
defects
dynamics
have
been
associated
with
numerous
human
diseases.
These
transitions
mainly
ensured
by
large
GTPases
belonging
Dynamin
family.
Mitochondrial
is
a
multi-step
process
allowing
division
one
mitochondrion
two
daughter
mitochondria.
It
regulated
recruitment
GTPase
Dynamin-related
protein
1
(Drp1)
adaptors
at
actin-
endoplasmic
reticulum-mediated
constriction
sites.
Drp1
oligomerization
followed
leads
2
terminate
membrane
scission.
Inner
has
proposed
be
an
independent
calcium
influx.
fusion
driven
two-step
outer
mediated
mitofusins
inner
optic
atrophy
1.
In
addition
role
lipid
composition,
several
members
can
undergo
post-translational
modifications
modulating
these
processes.
Understanding
molecular
mechanisms
controlling
decipher
how
shape
meets
function
increase
knowledge
on
basis
diseases
morphology
defects.
This
article
will
describe
overview
that
govern
mammals.
Signal Transduction and Targeted Therapy,
Journal Year:
2019,
Volume and Issue:
4(1)
Published: Aug. 23, 2019
Abstract
Alzheimer’s
disease
(AD)
is
a
neurodegenerative
characterized
by
progressive
memory
loss
along
with
neuropsychiatric
symptoms
and
decline
in
activities
of
daily
life.
Its
main
pathological
features
are
cerebral
atrophy,
amyloid
plaques,
neurofibrillary
tangles
the
brains
patients.
There
various
descriptive
hypotheses
regarding
causes
AD,
including
cholinergic
hypothesis,
tau
propagation
mitochondrial
cascade
calcium
homeostasis
neurovascular
inflammatory
metal
ion
lymphatic
system
hypothesis.
However,
ultimate
etiology
AD
remains
obscure.
In
this
review,
we
discuss
related
clinical
trials.
Wealthy
puzzles
lessons
have
made
it
possible
to
develop
explanatory
theories
identify
potential
strategies
for
therapeutic
interventions
AD.
The
combination
hypometabolism
autophagy
deficiency
likely
be
causative
factor
We
further
propose
that
fluoxetine,
selective
serotonin
reuptake
inhibitor,
has
treat
Antioxidants,
Journal Year:
2018,
Volume and Issue:
7(1), P. 13 - 13
Published: Jan. 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.
