Frontiers in Immunology,
Год журнала:
2024,
Номер
14
Опубликована: Янв. 8, 2024
Neutrophils
are
the
most
abundant
innate
immune
cells.
Multiple
mechanisms
allow
them
to
engage
a
wide
range
of
metabolic
pathways
for
biosynthesis
and
bioenergetics
mediating
biological
processes
such
as
development
in
bone
marrow
antimicrobial
activity
ROS
production
NET
formation,
inflammation
tissue
repair.
We
first
discuss
recent
work
on
neutrophil
functions
regulate
granulopoiesis,
migration
trafficking
well
effector
functions.
then
syndromes
with
impaired
that
influenced
by
genetic
environmental
factors
nutrient
availability
usage.
Here,
we
particularly
focus
role
specific
macronutrients,
glucose,
fatty
acids,
protein,
micronutrients
vitamin
B3,
regulating
biology
how
this
regulation
impacts
host
health.
A
special
section
review
primarily
discusses
ways
deficiencies
could
impact
increase
infection
susceptibility.
emphasize
biochemical
approaches
explore
metabolism
relation
Lastly,
opportunities
challenges
neutrophil-centered
therapeutic
immune-driven
diseases
highlight
unanswered
questions
guide
future
discoveries.
The Journal of Cell Biology,
Год журнала:
2017,
Номер
216(7), С. 2027 - 2045
Опубликована: Май 31, 2017
Mitochondrial
stress
activates
a
mitonuclear
response
to
safeguard
and
repair
mitochondrial
function
adapt
cellular
metabolism
stress.
Using
multiomics
approach
in
mammalian
cells
treated
with
four
types
of
stressors,
we
identify
activating
transcription
factor
4
(ATF4)
as
the
main
regulator
response.
Surprisingly,
canonical
unfolded
protein
genes
mediated
by
ATF5
are
not
activated.
Instead,
ATF4
expression
cytoprotective
genes,
which
reprogram
through
activation
integrated
(ISR).
promotes
local
proteostatic
reducing
ribosomal
proteins,
inhibiting
translation,
coupling
ISR
attenuation
function.
Through
trans–expression
quantitative
trait
locus
analysis,
provide
genetic
evidence
supporting
role
for
Fh1
control
Atf4
mammals.
gene
data
from
mice
humans
diseases,
show
that
pathway
is
activated
vivo
upon
Our
illustrate
value
characterize
complex
networks
versatile
resource
new
regulators
mitochondrial-related
diseases.
Signal Transduction and Targeted Therapy,
Год журнала:
2019,
Номер
4(1)
Опубликована: Авг. 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
Frontiers in Neuroendocrinology,
Год журнала:
2018,
Номер
49, С. 72 - 85
Опубликована: Янв. 12, 2018
Energy
is
required
to
sustain
life
and
enable
stress
adaptation.
At
the
cellular
level,
energy
largely
derived
from
mitochondria
–
unique
multifunctional
organelles
with
their
own
genome.
Four
main
elements
connect
stress:
(1)
at
molecular,
(epi)genetic,
cellular,
organellar,
systemic
levels
components
of
responses;
(2)
Glucocorticoids
other
steroid
hormones
are
produced
metabolized
by
mitochondria;
(3)
Reciprocally,
respond
neuroendocrine
metabolic
mediators;
(4)
Experimentally
manipulating
mitochondrial
functions
alters
physiological
behavioral
responses
psychological
stress.
Thus,
endocrine
that
provide
both
signals
direct
Neural
circuits
regulating
social
behavior
as
well
psychopathological
processes
also
influenced
energetics.
An
integrative
view
an
energy-driven
process
opens
new
opportunities
study
mechanisms
adaptation
regulation
across
lifespan.
AJP Endocrinology and Metabolism,
Год журнала:
2019,
Номер
316(2), С. E268 - E285
Опубликована: Янв. 2, 2019
Type
2
diabetes
mellitus
(T2DM)
is
a
systemic
disease
characterized
by
hyperglycemia,
hyperlipidemia,
and
organismic
insulin
resistance.
This
pathological
shift
in
both
circulating
fuel
levels
energy
substrate
utilization
central
peripheral
tissues
contributes
to
mitochondrial
dysfunction
across
organ
systems.
The
mitochondrion
lies
at
the
intersection
of
critical
cellular
pathways
such
as
metabolism,
reactive
oxygen
species
(ROS)
generation,
apoptosis.
It
disequilibrium
these
processes
T2DM
that
results
downstream
deficits
vital
functions,
including
hepatocyte
cardiac
output,
skeletal
muscle
contraction,
β-cell
production,
neuronal
health.
Although
mitochondria
are
known
be
susceptible
variety
genetic
environmental
insults,
accumulation
DNA
(mtDNA)
mutations
mtDNA
copy
number
depletion
helping
explain
prevalence
mitochondrial-related
diseases
T2DM.
Recent
work
has
uncovered
novel
biology
implicated
progressions
heteroplasmy,
noncoding
RNA
(ncRNA),
epigenetic
modification
genome,
epitranscriptomic
regulation
mtDNA-encoded
transcriptome.
goal
this
review
highlight
observed
throughout
major
systems
context
present
new
ideas
for
future
research
directions
based
on
experimental
technological
innovations
biology.
Finally,
field
mitochondria-targeted
therapeutics
discussed,
with
an
emphasis
therapeutic
strategies
restore
homeostasis
setting
International Journal of Molecular Sciences,
Год журнала:
2017,
Номер
18(6), С. 1126 - 1126
Опубликована: Май 24, 2017
Over
the
past
decades,
peroxisomes
have
emerged
as
key
regulators
in
overall
cellular
lipid
and
reactive
oxygen
species
metabolism.
In
mammals,
these
organelles
also
been
recognized
important
hubs
redox-,
lipid-,
inflammatory-,
innate
immune-signaling
networks.
To
exert
activities,
must
interact
both
functionally
physically
with
other
cell
organelles.
This
review
provides
a
comprehensive
look
of
what
is
currently
known
about
interconnectivity
between
mitochondria
within
mammalian
cells.
We
first
outline
how
peroxisomal
mitochondrial
abundance
are
controlled
by
common
sets
cis-
trans-acting
factors.
Next,
we
discuss
may
communicate
each
at
molecular
level.
addition,
reflect
on
cooperate
various
metabolic
signaling
pathways.
Finally,
address
why
to
maintain
healthy
relationship
defects
one
organelle
cause
dysfunction
other.
Gaining
better
insight
into
issues
pivotal
understanding
function
their
environment,
health
disease.
ABSTRACT
The
importance
of
mitochondria
in
energy
metabolism,
signal
transduction
and
aging
post-mitotic
tissues
has
been
well
established.
Recently,
the
crucial
role
mitochondrial-linked
signaling
stem
cell
function
come
to
light
mediating
activity
is
becoming
increasingly
recognized.
Despite
fact
that
many
cells
exhibit
low
mitochondrial
content
a
reliance
on
mitochondrial-independent
glycolytic
metabolism
for
energy,
accumulating
evidence
implicated
activation,
fate
decisions
defense
against
senescence.
In
this
Review,
we
discuss
recent
advances
link
homeostasis,
stress
responses,
dynamics
function,
particularly
context
disease
aging.
This
Review
will
also
highlight
some
progress
therapeutics
may
present
attractive
strategies
improving
as
basis
regenerative
medicine
healthy
International Journal of Molecular Sciences,
Год журнала:
2021,
Номер
22(21), С. 11338 - 11338
Опубликована: Окт. 20, 2021
Mitochondria
are
the
energy
center
of
cell.
They
found
in
cell
cytoplasm
as
dynamic
networks
where
they
adapt
production
based
on
cell’s
needs.
also
at
proinflammatory
response
and
have
essential
roles
against
pathogenic
infections.
a
major
site
for
Reactive
Oxygen
Species
(ROS;
or
free
radicals),
which
to
fight
infection.
However,
excessive
uncontrolled
can
become
deleterious
cell,
leading
mitochondrial
tissue
damage.
Pathogens
exploit
role
mitochondria
during
infection
by
affecting
oxidative
phosphorylation
mechanism
(OXPHOS),
network
disrupting
communication
between
nucleus
mitochondria.
The
these
biological
processes
makes
organelle
good
targets
development
therapeutic
strategies.
In
this
review,
we
presented
summary
endosymbiotic
origin
their
involvement
pathogen
response,
well
potential
promising
infectious
diseases
chronic
inflammatory
diseases.
