Biomolecules,
Journal Year:
2024,
Volume and Issue:
15(1), P. 33 - 33
Published: Dec. 30, 2024
Voltage-Dependent
Anion
Channel
1
(VDAC1)
is
a
mitochondrial
outer
membrane
protein
that
plays
crucial
role
in
regulating
cellular
energy
metabolism
and
apoptosis
by
mediating
the
exchange
of
ions
metabolites
between
mitochondria
cytosol.
Mitochondrial
dysfunction
oxidative
stress
are
central
features
neurodegenerative
diseases.
The
pivotal
functions
VDAC1
controlling
permeability,
calcium
balance,
facilitating
programmed
cell
death
pathways,
position
it
as
key
determinant
delicate
balance
neuronal
viability
degeneration.
Accordingly,
increasing
evidence
suggests
implicated
pathophysiology
diseases,
including
Alzheimer’s
disease
(AD),
Parkinson’s
(PD),
amyotrophic
lateral
sclerosis
(ALS),
others.
This
review
summarizes
current
findings
on
contribution
to
neurodegeneration,
focusing
its
interactions
with
disease-specific
proteins,
such
amyloid-β,
α-synuclein,
mutant
SOD1.
By
unraveling
complex
involvement
processes,
this
highlights
potential
avenues
for
future
research
drug
development
aimed
at
alleviating
mitochondrial-related
neurodegeneration.
Huntington's
disease
(HD)
is
a
devastating
neurodegenerative
that
manifested
by
gradual
loss
of
physical,
cognitive,
and
mental
abilities.
As
the
advances,
age
has
major
impact
on
pathogenic
signature
mutant
huntingtin
(mHTT)
protein
aggregation.
This
review
aims
to
explore
intricate
relationship
between
aging,
mHTT
toxicity,
cellular
senescence
in
HD.
Scientific
data
interplay
mHTT,
HD
were
collected
from
several
academic
databases,
including
PubMed,
Google
Scholar,
Google,
ScienceDirect.
The
search
terms
employed
"AGING,"
"HUNTINGTON'S
DISEASE,"
"MUTANT
HUNTINGTIN,"
"CELLULAR
SENESCENCE."
Additionally,
gather
information
molecular
mechanisms
potential
therapeutic
targets,
was
extended
include
relevant
such
as
"DNA
DAMAGE,"
"OXIDATIVE
STRESS,"
"AUTOPHAGY."
According
research,
aging
leads
worsening
pathophysiology
through
some
processes.
result
accumulation,
promoted,
which
causes
DNA
damage,
oxidative
stress,
decreased
autophagy,
increased
inflammatory
responses.
Pro-inflammatory
cytokines
other
substances
are
released
senescent
cells,
may
worsen
neuronal
damage
course
disease.
It
been
shown
treatments
directed
at
these
pathways
reduce
symptoms
enhance
longevity
experimental
animals,
pointing
new
possibility
treating
condition.
Through
their
amplification
harmful
effects
play
crucial
roles
development
Comprehending
interplays
creates
novel
opportunities
for
measures
targeted
alleviating
enhancing
patients'
quality
life.
Biomedicines,
Journal Year:
2025,
Volume and Issue:
13(3), P. 591 - 591
Published: Feb. 28, 2025
The
mechanisms
of
pathogenesis
hypertrophic
cardiomyopathy
are
associated
with
mutations
in
the
sarcomere
genes
cardiomyocytes
and
metabolic
disorders
cell,
including
mitochondrial
dysfunction.
Mitochondria
characterized
by
presence
their
own
DNA
enzyme
complexes
involved
oxidative
reactions,
which
cause
damage
to
protein
structures
membranes
reactive
oxygen
species.
Mitochondrial
dysfunctions
can
also
be
encoding
proteins
lead
a
violation
protective
functions
such
as
mitophagy,
fusion,
fission.
Mutations
myofibril
negatively
affect
mitochondria
through
increased
stress
due
an
need
for
ATP.
dysfunction
is
impaired
ATP
synthesis
cardiac
contractility,
leading
clinical
manifestations
cardiomyopathy.
current
review
was
designed
characterize
role
based
on
published
data;
search
publications
analysis
articles
keywords
“hypertrophic
cardiomyopathy,
mitochondria,
dysfunction”
PubMed
Scopus
databases
up
January
2025.
Frontiers in Immunology,
Journal Year:
2025,
Volume and Issue:
16
Published: April 15, 2025
Bezafibrate
(BEZ)
is
a
drug
used
to
treat
hypertriglyceridemia
and
its
long-term
use
has
been
associated
with
reduced
risk
of
cancer
in
patients
coronary
artery
disease.
Recent
studies
uncovered
that
BEZ
potent
modulator
mitochondrial
biogenesis
through
activation
PGC-1α/PPAR
complexes,
resulting
modulation
lipid
metabolism
fatty
acid
oxidation.
Mitochondria
impact
virtually
all
processes
linked
oncogenesis,
disruption
normal
bioenergetics
oxidative
phosphorylation
(OXPHOS)
occurs
early
during
oncogenesis
change
the
energy
cells
as
well
various
tumor
microenvironment
(TME).
Therefore,
we
synthesized
analog
(Mito-BEZ)
preferentially
localizes
mitochondria,
thereby
enabling
lower
doses
Mito-BEZ
than
achieve
greater
efficacy.
Our
demonstrate
significantly
more
at
inhibiting
LUAD
cell
growth
vitro
lung
tumorigenesis
preclinical
mouse
models.
was
also
>200-fold
both
complex
I
III
cells.
Furthermore,
suppresses
while
markedly
upregulating
function
effector
CD8+
T
cells,
immune
response
TME.
results
show
Mito-BEZ,
favorable
toxicity
profile,
exhibited
striking
inhibitory
effect
on
progression
metastasis
by
targeting
fundamental
difference
metabolic
plasticity
between
