Autophagy,
Journal Year:
2021,
Volume and Issue:
18(6), P. 1216 - 1239
Published: Sept. 29, 2021
Owing
to
the
dominant
functions
of
mitochondria
in
multiple
cellular
metabolisms
and
distinct
types
regulated
cell
death,
maintaining
a
functional
mitochondrial
network
is
fundamental
for
homeostasis
body
fitness
response
physiological
adaptations
stressed
conditions.
The
process
mitophagy,
which
dysfunctional
or
superfluous
are
selectively
engulfed
by
autophagosome
subsequently
degraded
lysosome,
has
been
well
formulated
as
one
major
mechanisms
quality
control.
To
date,
PINK1-PRKN-dependent
receptors
(including
proteins
lipids)-dependent
pathways
have
characterized
determine
mitophagy
mammalian
cells.
highly
responsive
dynamics
endogenous
metabolites,
including
iron-,
calcium-,
glycolysis-TCA-,
NAD+-,
amino
acids-,
fatty
cAMP-associated
metabolites.
Herein,
we
summarize
recent
advances
toward
molecular
details
regulation
We
also
highlight
key
regulations
shed
new
light
on
bidirectional
interplay
between
metabolisms,
with
attempting
provide
perspective
insight
into
nutritional
intervention
metabolic
disorders
deficit.
Frontiers in Aging Neuroscience,
Journal Year:
2021,
Volume and Issue:
13
Published: Feb. 18, 2021
Mitochondria
play
a
pivotal
role
in
bioenergetics
and
respiratory
functions,
which
are
essential
for
the
numerous
biochemical
processes
underpinning
cell
viability.
Mitochondrial
morphology
changes
rapidly
response
to
external
insults
metabolic
status
via
fission
fusion
(so-called
mitochondrial
dynamics)
that
maintain
quality
homeostasis.
Damaged
mitochondria
removed
by
process
known
as
mitophagy,
involves
their
degradation
specific
autophagosomal
pathway.
Over
last
few
years,
remarkable
efforts
have
been
made
investigate
impact
on
pathogenesis
of
Alzheimer's
disease
(AD)
various
forms
dysfunction,
such
excessive
reactive
oxygen
species
(ROS)
production,
Ca2+
dyshomeostasis,
loss
ATP,
defects
dynamics
transport,
mitophagy.
Recent
research
suggests
restoration
function
physical
exercise,
an
antioxidant
diet,
or
therapeutic
approaches
can
delay
onset
slow
progression
AD.
In
this
review,
we
focus
recent
progress
highlights
crucial
alterations
oxidative
stress
AD,
emphasizing
framework
existing
potential
approaches.
Cells,
Journal Year:
2019,
Volume and Issue:
8(8), P. 795 - 795
Published: July 30, 2019
Mitochondrial
uncoupling
can
be
defined
as
a
dissociation
between
mitochondrial
membrane
potential
generation
and
its
use
for
mitochondria-dependent
ATP
synthesis.
Although
this
process
was
originally
considered
dysfunction,
the
identification
of
UCP-1
an
endogenous
physiological
protein
suggests
that
could
involved
in
many
other
biological
processes.
In
review,
we
first
compare
agents
available
term
mechanistic
non-specific
effects.
Proteins
regulating
uncoupling,
well
chemical
compounds
with
properties
are
discussed.
Second,
summarize
most
recent
findings
linking
cellular
or
processes,
such
bulk
specific
autophagy,
reactive
oxygen
species
production,
secretion,
cell
death,
physical
exercise,
metabolic
adaptations
adipose
tissue,
signaling.
Finally,
show
how
used
to
treat
several
human
diseases,
obesity,
cardiovascular
neurological
disorders.
Oxidative Medicine and Cellular Longevity,
Journal Year:
2020,
Volume and Issue:
2020, P. 1 - 11
Published: Feb. 18, 2020
Almost
all
human
diseases
are
strongly
associated
with
inflammation,
and
a
deep
understanding
of
the
exact
mechanism
is
helpful
for
treatment.
The
NLRP3
inflammasome
composed
protein,
procaspase-1,
ASC
plays
vital
role
in
regulating
inflammation.
In
this
review,
regulation
activation,
its
proinflammatory
inflammatory
diseases,
interactions
autophagy,
targeted
therapeutic
approaches
will
be
summarized.
International Journal of Molecular Sciences,
Journal Year:
2020,
Volume and Issue:
21(21), P. 8323 - 8323
Published: Nov. 6, 2020
Calcium
(Ca2+)
is
a
major
second
messenger
in
cells
and
essential
for
the
fate
survival
of
all
higher
organisms.
Different
Ca2+
channels,
pumps,
or
exchangers
regulate
variations
duration
levels
intracellular
Ca2+,
which
may
be
transient
sustained.
These
changes
are
then
decoded
by
an
elaborate
toolkit
Ca2+-sensors,
translate
signal
to
operational
cell
machinery,
thereby
regulating
numerous
Ca2+-dependent
physiological
processes.
Alterations
homoeostasis
signaling
often
deleterious
associated
with
certain
pathological
states,
including
cancer.
Altered
transmission
has
been
implicated
variety
processes
fundamental
uncontrolled
proliferation
invasiveness
tumor
other
important
cancer
progression,
such
as
development
resistance
therapies.
Here,
we
review
what
known
about
how
this
regulates
life
death
decisions
context
cancer,
particular
attention
directed
proliferation,
apoptosis,
autophagy.
We
also
explore
intersections
therapeutic
targeting
cells,
summarizing
opportunities
modulators
improve
effectiveness
current
anticancer
Signal Transduction and Targeted Therapy,
Journal Year:
2024,
Volume and Issue:
9(1)
Published: May 15, 2024
Abstract
Mitochondria,
with
their
intricate
networks
of
functions
and
information
processing,
are
pivotal
in
both
health
regulation
disease
progression.
Particularly,
mitochondrial
dysfunctions
identified
many
common
pathologies,
including
cardiovascular
diseases,
neurodegeneration,
metabolic
syndrome,
cancer.
However,
the
multifaceted
nature
elusive
phenotypic
threshold
dysfunction
complicate
our
understanding
contributions
to
diseases.
Nonetheless,
these
complexities
do
not
prevent
mitochondria
from
being
among
most
important
therapeutic
targets.
In
recent
years,
strategies
targeting
have
continuously
emerged
transitioned
clinical
trials.
Advanced
intervention
such
as
using
healthy
replenish
or
replace
damaged
mitochondria,
has
shown
promise
preclinical
trials
various
Mitochondrial
components,
mtDNA,
mitochondria-located
microRNA,
associated
proteins
can
be
potential
agents
augment
function
immunometabolic
diseases
tissue
injuries.
Here,
we
review
current
knowledge
pathophysiology
concrete
examples
We
also
summarize
treat
perspective
dietary
supplements
targeted
therapies,
well
translational
situation
related
pharmacology
agents.
Finally,
this
discusses
innovations
applications
transplantation
an
advanced
promising
treatment.
Proceedings of the National Academy of Sciences,
Journal Year:
2020,
Volume and Issue:
117(32), P. 19266 - 19275
Published: July 23, 2020
Significance
Mitochondria
and
lysosomes
are
critical
for
cellular
homeostasis
defects
in
both
organelles
observed
several
diseases.
Recently,
contact
sites
between
mitochondria
were
identified
found
to
modulate
mitochondrial
dynamics.
However,
whether
mitochondria–lysosome
contacts
have
additional
functions
is
unknown.
Here,
we
identify
a
function
of
facilitating
the
direct
transfer
calcium
from
mitochondria.
Transfer
at
mediated
by
lysosomal
channel
TRPML1
disrupted
mucolipidosis
type
IV,
storage
disorder
caused
loss-of-function
mutations
TRPML1.
Calcium
thus
presents
an
mechanism
intracellular
regulation
that
may
further
contribute
various
disorders.
Cold Spring Harbor Perspectives in Biology,
Journal Year:
2019,
Volume and Issue:
12(1), P. a038802 - a038802
Published: Aug. 19, 2019
Martin
D.
Bootman1
and
Geert
Bultynck2
1School
of
Life,
Health
Chemical
Sciences,
The
Open
University,
Milton
Keynes
MK7
6AA,
United
Kingdom
2Laboratory
Molecular
Cellular
Signaling,
Department
Medicine,
KU
Leuven,
B-3000
Belgium
Correspondence:
martin.bootman{at}open.ac.uk
