Aging and Disease,
Год журнала:
2024,
Номер
unknown, С. 0 - 0
Опубликована: Янв. 1, 2024
Mitochondrial
dysfunction
plays
a
pivotal
role
in
the
development
of
age-related
diseases,
particularly
neurodegenerative
disorders.
The
etiology
mitochondrial
involves
multitude
factors
that
remain
elusive.
This
review
centers
on
elucidating
role(s)
excitotoxicity,
oxytosis/ferroptosis
and
neurodegeneration
within
context
bioenergetics,
biogenesis,
mitophagy
oxidative
stress
explores
their
intricate
interplay
pathogenesis
diseases.
effective
coordination
turnover
processes,
notably
is
assumed
to
be
critically
important
for
cellular
resilience
longevity.
However,
age-associated
decrease
impedes
elimination
dysfunctional
mitochondria,
consequently
impairing
biogenesis.
deleterious
cascade
results
accumulation
damaged
mitochondria
deterioration
functions.
Both
excitotoxicity
have
been
demonstrated
contribute
significantly
pathophysiology
including
Alzheimer's
disease
(AD),
Parkinson's
(PD),
Huntington's
Disease
(HD),
Amyotrophic
Lateral
Sclerosis
(ALS)
Multiple
(MS).
Excitotoxicity,
characterized
by
excessive
glutamate
signaling,
initiates
events
involving
calcium
dysregulation,
energy
depletion,
intricately
linked
dysfunction.
Furthermore,
emerging
concepts
surrounding
underscore
importance
iron-dependent
lipid
peroxidation
engagement
neurodegeneration.
not
only
discusses
individual
contributions
ferroptosis
but
also
emphasizes
convergence
with
dysfunction,
key
driver
Understanding
crosstalk
between
oxytosis/ferroptosis,
holds
potential
pave
way
mitochondrion-targeted
therapeutic
strategies.
Such
strategies,
focus
mitophagy,
stress,
emerge
as
promising
avenues
intervention.
Acta Pharmaceutica Sinica B,
Год журнала:
2022,
Номер
12(6), С. 2778 - 2789
Опубликована: Март 10, 2022
Neurodegenerative
diseases
(NDDs)
such
as
Alzheimer's
disease
(AD)
and
Parkinson's
(PD)
are
a
heterogeneous
group
of
disorders
characterized
by
progressive
degeneration
neurons.
NDDs
threaten
the
lives
millions
people
worldwide
regretfully
remain
incurable.
It
is
well
accepted
that
dysfunction
mitochondria
underlies
pathogenesis
NDDs.
Dysfunction
results
in
energy
depletion,
oxidative
stress,
calcium
overloading,
caspases
activation,
which
dominates
neuronal
death
Therefore,
preferred
target
for
intervention
So
far
various
mitochondria-targeting
drugs
have
been
developed
delightfully
some
them
demonstrate
promising
outcome,
though
there
still
obstacles
targeting
specificity,
delivery
capacity
hindering
development.
In
present
review,
we
will
elaborately
address
1)
strategy
to
design
drugs,
2)
rescue
mechanism
respective
3)
how
evaluate
therapeutic
effect.
Hopefully
this
review
provide
comprehensive
knowledge
understanding
develop
more
effective
treatment
Behavioural Brain Research,
Год журнала:
2024,
Номер
463, С. 114889 - 114889
Опубликована: Фев. 1, 2024
Alzheimer's
disease
(AD)
is
the
most
prevalent
form
of
dementia,
characterized
by
severe
mitochondrial
dysfunction,
which
an
intracellular
process
that
significantly
compromised
in
early
stages
AD.
Mitophagy,
selective
removal
damaged
mitochondria,
a
potential
therapeutic
strategy
for
Rapamycin,
mammalian
target
rapamycin
(mTOR)
inhibitor,
augmented
autophagy
and
mitigated
cognitive
impairment.
Our
study
revealed
enhances
function
activating
mitophagy,
alleviating
neuronal
loss,
improving
dysfunction
5
×FAD
mice.
Interestingly,
neuroprotective
effect
AD
were
negated
treatment
with
3-MA,
mitophagy
inhibitor.
Overall,
our
findings
suggest
ameliorates
impairment
mice
via
activation
its
downstream
PINK1-Parkin
pathway,
aids
clearance
amyloid-β
(Aβ)
mitochondria.
This
reveals
novel
mechanism
involving
regulation
underlying
provides
new
insights
targets
However,
there
are
still
some
shortcomings
this
topic;
if
we
can
further
knock
out
PINK1/Parkin
gene
animals
or
use
siRNA
technology,
confirm
experimental
results.
Frontiers in Endocrinology,
Год журнала:
2022,
Номер
13
Опубликована: Авг. 11, 2022
Berberine
is
a
natural
active
ingredient
extracted
from
the
rhizome
of
Rhizoma
Coptidis
,
which
interacts
with
multiple
intracellular
targets
and
exhibits
wide
range
pharmacological
activities.
Previous
studies
have
preliminarily
confirmed
that
regulation
mitochondrial
activity
related
to
various
actions
berberine,
such
as
regulating
blood
sugar
lipid
inhibiting
tumor
progression.
However,
mechanism
berberine’s
remains
be
further
studied.
This
paper
summarizes
molecular
quality
control
system
briefly
reviews
berberine
in
activity.
It
proposed
mainly
regulates
glycolipid
metabolism
by
respiratory
chain
function,
promotes
cell
apoptosis
pathway,
protects
cardiac
function
promoting
mitophagy
alleviate
dysfunction.
reveals
effects
perspective
mitochondria
provides
scientific
basis
for
application
clinical
treatment
diseases.
