Frontiers in Cellular and Infection Microbiology,
Journal Year:
2023,
Volume and Issue:
13
Published: June 14, 2023
The
bacterial
origin
of
mitochondria
has
been
a
widely
accepted
as
an
event
that
occurred
about
1.45
billion
years
ago
and
endowed
cells
with
internal
energy
producing
organelle.
Thus,
have
traditionally
viewed
subcellular
organelle
any
other
–
fully
functionally
dependent
on
the
cell
it
is
part
of.
However,
recent
studies
given
us
evidence
are
more
independent
than
organelles,
they
can
function
outside
cells,
engage
in
complex
“social”
interactions,
communicate
each
well
cellular
components,
bacteria
viruses.
Furthermore,
move,
assemble
organize
upon
sensing
different
environmental
cues,
using
process
akin
to
quorum
sensing.
Therefore,
taking
all
these
lines
into
account
we
hypothesize
need
be
studied
from
perspective
entity.
This
view
may
lead
new
insights
their
biological
function,
inform
strategies
for
treatment
disease
associated
mitochondrial
dysfunction.
Cell Metabolism,
Journal Year:
2022,
Volume and Issue:
34(11), P. 1620 - 1653
Published: Nov. 1, 2022
The
analogy
of
mitochondria
as
powerhouses
has
expired.
Mitochondria
are
living,
dynamic,
maternally
inherited,
energy-transforming,
biosynthetic,
and
signaling
organelles
that
actively
transduce
biological
information.
We
argue
the
processor
cell,
together
with
nucleus
other
they
constitute
mitochondrial
information
processing
system
(MIPS).
In
a
three-step
process,
(1)
sense
respond
to
both
endogenous
environmental
inputs
through
morphological
functional
remodeling;
(2)
integrate
network-based
physical
interactions
diffusion
mechanisms;
(3)
produce
output
signals
tune
functions
systemically
regulate
physiology.
This
input-to-output
transformation
allows
metabolic,
biochemical,
neuroendocrine,
local
or
systemic
enhance
organismal
adaptation.
An
explicit
focus
on
signal
transduction
emphasizes
role
communication
in
biology.
framework
also
opens
new
avenues
understand
how
mediate
inter-organ
processes
underlying
human
health.
Journal of Hematology & Oncology,
Journal Year:
2022,
Volume and Issue:
15(1)
Published: July 18, 2022
Drug
resistance
represents
a
major
obstacle
in
cancer
management,
and
the
mechanisms
underlying
stress
adaptation
of
cells
response
to
therapy-induced
hostile
environment
are
largely
unknown.
As
central
organelle
for
cellular
energy
supply,
mitochondria
can
rapidly
undergo
dynamic
changes
integrate
signaling
pathways
provide
bioenergetic
biosynthetic
flexibility
cells,
which
contributes
multiple
aspects
tumor
characteristics,
including
drug
resistance.
Therefore,
targeting
therapy
overcoming
has
attracted
increasing
attention
various
types
cancer.
Multiple
mitochondrial
processes,
dynamics,
metabolism,
apoptotic
regulatory
machinery,
have
been
demonstrated
be
potential
targets.
However,
recent
insights
into
revealed
complexity
structure
functions,
elusive
functions
biology,
inaccessibility
mitochondria,
posed
challenges
clinical
application
mitochondrial-based
therapeutic
strategies.
discovery
both
novel
mitochondria-targeting
agents
innovative
approaches
is
urgently
required.
Here,
we
review
most
literature
summarize
molecular
their
intricate
connection
with
In
addition,
an
overview
emerging
strategies
target
effectively
chemoresistance
highlighted,
emphasis
on
repositioning
delivery
approaches,
may
accelerate
compounds
therapy.
Biomolecules,
Journal Year:
2022,
Volume and Issue:
12(3), P. 427 - 427
Published: March 10, 2022
Mitochondria,
the
cell’s
major
energy
producers,
also
act
as
signaling
hubs,
interacting
with
other
organelles
both
directly
and
indirectly.
Despite
having
its
own
circular
genome,
majority
of
mitochondrial
proteins
are
encoded
by
nuclear
DNA.
To
respond
to
changes
in
cell
physiology,
mitochondria
must
send
signals
nucleus,
which
can,
turn,
upregulate
gene
expression
alter
metabolism
or
initiate
a
stress
response.
This
is
known
retrograde
signaling.
A
variety
stimuli
pathways
fall
under
umbrella.
Mitochondrial
dysfunction
has
already
been
shown
have
severe
implications
for
human
health.
Disruption
signaling,
whether
associated
cellular
environmental
changes,
may
contribute
pathological
deficits.
In
this
review,
we
discuss
between
examine
possibility
direct
contacts,
identify
consequences
an
altered
relationship.
Trends in Neurosciences,
Journal Year:
2023,
Volume and Issue:
46(2), P. 137 - 152
Published: Jan. 10, 2023
Efforts
to
understand
how
mitochondrial
dysfunction
contributes
neurodegeneration
have
primarily
focussed
on
the
role
of
mitochondria
in
neuronal
energy
metabolism.
However,
progress
understanding
etiological
nature
emerging
functions
has
yielded
new
ideas
about
basis
neurological
disease.
Studies
aimed
at
deciphering
signal
through
interorganellar
contacts,
vesicular
trafficking,
and
metabolic
transmission
revealed
that
regulation
immunometabolism,
cell
death,
organelle
dynamics,
neuroimmune
interplay
are
critical
determinants
neural
health.
Moreover,
homeostatic
mechanisms
exist
protect
health
turnover
via
nanoscale
proteostasis
lysosomal
degradation
become
integrated
within
signalling
pathways
support
plasticity
stress
responses
nervous
system.
This
review
highlights
these
distinct
converge
influence
contribute
disease
pathology.
Pharmacology & Therapeutics,
Journal Year:
2021,
Volume and Issue:
234, P. 108048 - 108048
Published: Nov. 28, 2021
Translocator
Protein
18
kDa
(TSPO),
previously
named
Peripheral
Benzodiazepine
Receptor,
is
a
well-validated
and
widely
used
biomarker
of
neuroinflammation
to
assess
diverse
central
nervous
system
(CNS)
pathologies
in
preclinical
clinical
studies.
Many
studies
have
shown
that
animal
models
human
neurological
neurodegenerative
disease
the
condition,
TSPO
levels
increase
brain
neuropil,
this
driven
by
infiltration
peripheral
inflammatory
cells
activation
glial
cells.
Therefore,
clear
understanding
dynamics
cellular
sources
response
critically
important
interpretation
Positron
Emission
Tomography
(PET)
for
pathophysiology
CNS
diseases.
Within
normal
compartment,
there
are
tissues
such
as
choroid
plexus,
ependymal
lining
ventricles,
vascular
endothelial
also
express
at
even
higher
than
However,
paucity
knowledge
if
these
cell
types
respond
diseased
brain.
These
do
provide
background
signal
needs
be
accounted
TSPO-PET
imaging
More
recently,
reports
may
expressed
neurons
adult
expression
increased
neuronal
activity.
it
essential
study
topic
with
great
deal
detail,
methodological
rigor,
rule
out
alternative
interpretations
artifacts.
High
present
outer
mitochondrial
membrane.
Recent
provided
evidence
its
localization
other
compartments
including
plasma
membrane
perinuclear
regions
which
define
functions
different
from
mitochondria.
A
greater
subcellular
infiltrating
immune
associated
function(s)
an
additional
layer
information
neurobiology.
This
review
effort
outline
recent
advances
examine
remaining
questions
require
rigorous
investigation.
Cancers,
Journal Year:
2021,
Volume and Issue:
13(13), P. 3311 - 3311
Published: July 1, 2021
Carcinogenesis
is
a
multi-step
process
that
refers
to
transformation
of
normal
cell
into
tumoral
neoplastic
cell.
The
mechanisms
promote
tumor
initiation,
promotion
and
progression
are
varied,
complex
remain
be
understood.
Studies
have
highlighted
the
involvement
oncogenic
mutations,
genomic
instability
epigenetic
alterations
as
well
metabolic
reprogramming,
in
different
processes
oncogenesis.
However,
underlying
still
clarified.
Mitochondria
central
organelles
at
crossroad
various
energetic
metabolisms.
In
addition
their
pivotal
roles
bioenergetic
metabolism,
they
control
redox
homeostasis,
biosynthesis
macromolecules
apoptotic
signals,
all
which
linked
carcinogenesis.
present
review,
we
discuss
how
mitochondria
contribute
initiation
carcinogenesis
through
gene
mutations
production
oncometabolites,
reprogramming
mitochondrial
dynamics.
Finally,
metabolism
promising
target
for
development
novel
therapeutic
strategies.
European Journal of Cell Biology,
Journal Year:
2022,
Volume and Issue:
101(3), P. 151225 - 151225
Published: April 13, 2022
Metabolic
alterations
have
been
observed
in
many
cancer
types.
The
deregulated
metabolism
has
thus
become
an
emerging
hallmark
of
the
disease,
where
is
frequently
rewired
to
aerobic
glycolysis.
This
led
concept
"metabolic
reprogramming",
which
therefore
extensively
studied.
Over
years,
it
characterized
enhancement
glycolysis,
key
mutations
some
enzymes
TCA
cycle,
and
increased
glucose
uptake,
are
used
by
cells
achieve
a
phenotype"
useful
gain
proliferation
advantage.
Many
studies
highlighted
detail
signaling
pathways
molecular
mechanisms
responsible
for
glycolytic
switch.
However,
glycolysis
not
only
metabolic
process
that
rely
on.
Oxidative
Phosphorylation
(OXPHOS),
gluconeogenesis
or
beta-oxidation
fatty
acids
(FAO)
may
be
involved
development
progression
several
tumors.
In
cases,
these
metabolisms
even
more
crucial
than
tumor
survival.
review
will
focus
on
contribution
survival
cancers.
We
also
analyze
balance
between
processes
regulated,
as
well
therapeutical
approaches
can
derive
from
their
study.