Frontiers in Molecular Biosciences,
Journal Year:
2022,
Volume and Issue:
9
Published: Nov. 7, 2022
Intervertebral
disc
degeneration
(IDD)
is
the
primary
cause
of
intervertebral
(IVD)
disease.
With
increased
ageing
society,
an
increasing
number
patients
are
plagued
by
Ageing
not
only
accelerates
decreased
vitality
and
functional
loss
cells
but
also
increases
intracellular
oxidative
stress.
Moreover,
speed
linked
to
high
levels
reactive
oxygen
species
(ROS)
production.
Not
production
ROS
in
cells,
antioxidant
degenerative
discs
decrease.
In
addition
disc,
structural
components
matrix
vulnerable
damage.
After
chronic
mitochondrial
dysfunction,
can
be
produced
large
quantities,
while
autophagy
eliminate
these
impaired
mitochondria
reduce
ROS.
Oxidative
stress
has
a
marked
impact
on
occurrence
IDD.
future,
IDD
treatment
aiming
improve
regulating
redox
balance
cells.
summary,
promote
IVD,
further
basic
clinical
trials
needed
determine
how
treat
At
present,
although
there
many
in-depth
studies
relationship
between
specific
mechanism
been
elucidated.
this
paper,
main
causes
diseases
studied
summarized,
studied.
Experimental & Molecular Medicine,
Journal Year:
2021,
Volume and Issue:
53(7), P. 1124 - 1133
Published: July 1, 2021
Intervertebral
disc
degeneration
(IDD)
is
a
common
and
early-onset
pathogenesis
in
the
human
lifespan
that
can
increase
risk
of
low
back
pain.
More
clarification
molecular
mechanisms
associated
with
onset
progression
IDD
likely
to
help
establish
novel
preventive
therapeutic
strategies.
Recently,
mitochondria
have
been
increasingly
recognized
as
participants
regulating
glycolytic
metabolism,
which
has
historically
regarded
main
metabolic
pathway
intervertebral
discs
due
their
avascular
properties.
Indeed,
mitochondrial
structural
functional
disruption
observed
degenerated
nucleus
pulposus
(NP)
cells
discs.
Multilevel
well-orchestrated
strategies,
namely,
quality
control
(MQC),
are
involved
maintenance
integrity,
proteostasis,
antioxidant
system,
dynamics,
mitophagy,
biogenesis.
Here,
we
address
key
evidence
current
knowledge
role
function
process
consider
how
MQC
strategies
contribute
protective
detrimental
properties
NP
cell
function.
The
relevant
potential
treatments
targeting
for
intervention
also
summarized.
Further
synergistic
among
may
provide
useful
clues
use
developing
treatments.
Orthopaedic Surgery,
Journal Year:
2022,
Volume and Issue:
14(8), P. 1569 - 1582
Published: June 8, 2022
Intervertebral
disc
degeneration
(IVDD)
is
the
most
common
contributor
to
low
back
pain
(LBP).
Recent
studies
have
found
that
oxidative
stress
and
reactive
oxygen
species
(ROS)
play
an
important
role
in
IVDD.
As
a
by‐product
of
aerobic
respiration,
ROS
mainly
produced
mitochondria
by
electron
transport
chain
other
mitochondrial
located
proteins.
With
excessive
accumulation
ROS,
are
also
primary
target
attack
cells.
A
disrupted
balance
between
intracellular
production
antioxidant
capacity
will
lead
stress,
which
key
cell
apoptosis,
senescence,
autophagy,
dysfunction.
pivotal
ingredient
dysfunction
manifests
as
imbalanced
dynamics
dysregulated
mitophagy.
Mitochondria
can
alter
their
own
through
process
fusion
fission,
so
disabled
be
separated
from
pool.
Moreover,
mitophagy
participates
clearing
these
dysfunctional
mitochondria.
Abnormality
any
processes
either
increases
or
decreases
clearance
leading
vicious
cycle
results
death
intervertebral
cells
large
quantities,
combined
with
degradation
extracellular
matrix
overproduction
metalloproteinase.
In
this
review,
we
explain
changes
morphology
function
during
stress‐mediated
IVDD
highlight
process.
Eventually,
summarize
therapeutic
strategies
targeting
based
on
current
understanding
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
14
Published: Jan. 11, 2024
Mitochondria
are
critical
for
cellular
energetic
metabolism,
intracellular
signaling
orchestration
and
programmed
death
regulation.
Therefore,
mitochondrial
dysfunction
is
associated
with
various
pathogeneses.
The
maintenance
of
homeostasis
functional
recovery
after
injury
coordinated
by
biogenesis,
dynamics
autophagy,
which
collectively
referred
to
as
quality
control.
There
increasing
evidence
that
mitochondria
important
targets
melatonin
exert
protective
effects
under
pathological
conditions.
Melatonin,
an
evolutionarily
conserved
tryptophan
metabolite,
can
be
synthesized,
transported
metabolized
in
mitochondria.
In
this
review,
we
summarize
the
role
damaged
elimination
energy
supply
regulating
control,
may
provide
new
strategies
clinical
treatment
mitochondria-related
diseases.
Drug Design Development and Therapy,
Journal Year:
2020,
Volume and Issue:
Volume 14, P. 2047 - 2060
Published: May 1, 2020
Autophagy
caused
by
ischemia/reperfusion
(I/R)
increases
the
extent
of
cardiomyocyte
damage.
Melatonin
(Mel)
diminishes
cardiac
injury
through
regulating
autophagy
and
mitochondrial
dynamics.
However,
illustrating
specific
role
mitophagy
in
cardioprotective
effects
melatonin
remains
a
challenge.
The
aim
our
research
was
to
investigate
impact
underlying
mechanisms
connection
with
during
anoxia/reoxygenation
(A/R)
H9c2
cells.H9c2
cells
were
pretreated
or
without
membrane
receptor
2
(MT2)
antagonist
4-P-PDOT,
MT2
agonist
IIK7
sirtuin
3
(SIRT3)
inhibitor
3-TYP
for
4
hours
then
subjected
A/R
injury.
Cell
viability,
cellular
apoptosis,
necrosis
levels
oxidative
markers
assessed.
expression
SIRT3
forkhead
box
O3a
(FoxO3a),
function
mitophagy-related
proteins
also
evaluated.A/R
provoked
enhanced
myocytes.
In
addition,
increased
correlated
decreased
stress
dysfunction
cells.
pretreatment
notably
cell
survival
apoptosis
response
after
injury,
accompanied
restored
function.
inhibition
excessive
is
involved
melatonin,
as
shown
molecules
Parkin,
Beclin1,
BCL2-interacting
protein
3-like
(BNIP3L,
best
known
NIX)
light
chain
II/light
I
(LC3
II/LC3
I)
ratio
upregulation
p62
expression.
Moreover,
FoxO3a
A/R-injured
abrogated
but
these
beneficial
attenuated
4-P-PDOT
IIK7.These
results
indicate
that
protects
suppressing
activating
MT2/SIRT3/FoxO3a
pathway.
may
be
useful
candidate
alleviating
myocardial
(MI/R)
future,
might
become
therapeutic
target.
Journal of Neurology and Psychology,
Journal Year:
2019,
Volume and Issue:
7(1), P. 01 - 09
Published: Dec. 12, 2019
Starting
from
the
macro-category
"sleep-wake
disorders",
as
defined
in
DSM-V,
individual
pathological
conditions
were
defined,
focusing
on
contextual
and
clinical
aspects,
to
continue
analysis
neural
correlates
strategic
therapy
be
used
solve
problems
encountered.
Molecules,
Journal Year:
2020,
Volume and Issue:
25(19), P. 4410 - 4410
Published: Sept. 25, 2020
Fighting
infectious
diseases,
particularly
viral
infections,
is
a
demanding
task
for
human
health.
Targeting
the
pathogens
or
targeting
host
are
different
strategies,
but
with
an
identical
purpose,
i.e.,
to
curb
pathogen’s
spreading
and
cure
illness.
It
appears
that
increase
tolerance
against
can
be
of
substantial
advantage
strategy
used
in
evolution.
Practically,
it
has
broader
protective
spectrum
than
only
specific
pathogens,
which
differ
terms
susceptibility.
Methods
applied
one
pandemic
even
effective
upcoming
pandemics
pathogens.
This
more
urgent
if
we
consider
possible
concomitance
two
respiratory
diseases
potential
multi-organ
afflictions
such
as
Coronavirus
disease
2019
(COVID-19)
seasonal
flu.
Melatonin
molecule
enhance
host’s
pathogen
invasions.
Due
its
antioxidant,
anti-inflammatory,
immunoregulatory
activities,
melatonin
capacity
reduce
severity
mortality
deadly
virus
infections
including
COVID-19.
synthesized
functions
mitochondria,
play
critical
role
infections.
Not
surprisingly,
synthesis
become
target
strategies
manipulate
mitochondrial
status.
For
example,
infection
switch
energy
metabolism
from
respiration
widely
anaerobic
glycolysis
plenty
oxygen
available
(the
Warburg
effect)
when
cell
cannot
generate
acetyl-coenzyme
A,
metabolite
required
biosynthesis.
Under
some
conditions,
aging,
gender,
predisposed
health
already
compromised
exposed
further
challenges,
lose
their
producing
sufficient
amounts
melatonin.
leads
reduced
support
makes
these
individuals
vulnerable
diseases.
Thus,
maintenance
function
by
supplementation
expected
beneficial
effects
on
outcome