Frontiers in Cellular and Infection Microbiology,
Год журнала:
2025,
Номер
14
Опубликована: Янв. 21, 2025
Mitochondrial
genomic
stability
is
critical
to
prevent
various
human
inflammatory
diseases.
Bacterial
infection
significantly
increases
oxidative
stress,
driving
mitochondrial
instability
and
initiating
disease.
Oxidative
DNA
base
damage
predominantly
repaired
by
excision
repair
(BER)
in
the
nucleus
(nBER)
as
well
mitochondria
(mtBER).
In
this
review,
we
summarize
molecular
mechanisms
of
spontaneous
H.
pylori
infection-associated
mtDNA
damage,
replication
its
impact
on
innate
immune
signaling.
Additionally,
discuss
how
mutations
located
targeting
sequence
(MTS)
BER
genes
may
contribute
genome
signaling
activation.
Overall,
review
summarizes
evidence
understand
dynamics
mtBER
response
during
-associated
pathological
outcomes.
International Journal of Molecular Sciences,
Год журнала:
2023,
Номер
24(17), С. 13033 - 13033
Опубликована: Авг. 22, 2023
Neurodegenerative
diseases
(NDs)
are
a
diverse
group
of
disorders
characterized
by
the
progressive
degeneration
and
death
neurons,
leading
to
range
neurological
symptoms.
Despite
heterogeneity
these
conditions,
common
denominator
is
implication
mitochondrial
dysfunction
in
their
pathogenesis.
Mitochondria
play
crucial
role
creating
biomolecules,
providing
energy
through
adenosine
triphosphate
(ATP)
generated
oxidative
phosphorylation
(OXPHOS),
producing
reactive
oxygen
species
(ROS).
When
they’re
not
functioning
correctly,
becoming
fragmented
losing
membrane
potential,
they
contribute
diseases.
In
this
review,
we
explore
how
mitochondria
fuse
undergo
fission,
especially
context
NDs.
We
discuss
genetic
protein
mutations
linked
impact
dynamics.
also
look
at
key
regulatory
proteins
fusion
(MFN1,
MFN2,
OPA1)
fission
(DRP1
FIS1),
including
post-translational
modifications.
Furthermore,
highlight
potential
drugs
that
can
influence
By
unpacking
complex
processes,
aim
direct
research
towards
treatments
improve
life
quality
for
people
with
challenging
conditions.
Ageing Research Reviews,
Год журнала:
2024,
Номер
99, С. 102357 - 102357
Опубликована: Июнь 1, 2024
Neurodegenerative
disorders
(NDs)
are
expected
to
pose
a
significant
challenge
for
both
medicine
and
public
health
in
the
upcoming
years
due
global
demographic
changes.
NDs
mainly
represented
by
degeneration/loss
of
neurons,
which
is
primarily
accountable
severe
mental
illness.
This
neuronal
degeneration
leads
many
neuropsychiatric
problems
permanent
disability
an
individual.
Moreover,
tight
junction
brain,
blood-brain
barrier
(BBB)has
protective
feature,
functioning
as
biological
that
can
prevent
medicines,
toxins,
foreign
substances
from
entering
brain.
However,
delivering
any
medicinal
agent
brain
(i.e.,
Multiple
sclerosis,
Alzheimer's,
Parkinson's,
etc.)
enormously
challenging.
There
approved
therapies
address
NDs,
but
most
them
only
help
treat
associated
manifestations.
The
available
have
failed
control
progression
certain
factors,
i.e.,
BBB
drug-associated
undesirable
effects.
extremely
complex
pathology,
with
pathogenic
mechanisms
involved
initiation
progression;
thereby,
limited
survival
rate
has
been
observed
ND
patients.
Hence,
understanding
exact
mechanism
behind
crucial
developing
alternative
approaches
improving
patients'
rates.
Thus,
present
review
sheds
light
on
different
cellular
novel
therapeutic
their
clinical
relevance,
will
assist
researchers
alternate
strategies
limitations
conventional
therapies.
current
work
offers
scope
into
near
future
improve
approach
NDs.
Frontiers in Cellular and Infection Microbiology,
Год журнала:
2024,
Номер
14
Опубликована: Фев. 16, 2024
Abnormal
behavior
of
α-synuclein
and
prion
proteins
is
the
hallmark
Parkinson’s
disease
(PD)
illnesses,
respectively,
being
complex
neurological
disorders.
A
primary
cause
protein
aggregation,
brain
injury,
cognitive
loss
in
illnesses
misfolding
normal
cellular
(PrP
C
)
into
an
infectious
form
Sc
).
Aggregation
causes
disruptions
processes
(PD),
leading
to
dopamine-producing
neurons
motor
symptoms.
Alteration
composition
or
activity
gut
microbes
may
weaken
intestinal
barrier
make
it
possible
for
prions
go
from
brain.
The
gut-brain
axis
linked
neuroinflammation;
metabolites
produced
by
microbiota
affect
aggregation
α-synuclein,
regulate
inflammation
immunological
responses,
influence
course
neurotoxicity
proteins,
even
if
their
targets
are
distinct
proteins.
This
thorough
analysis
explores
interactions
that
exist
between
neurodegenerative
particularly
involvement
microbiota,
a
collection
bacteria,
archaea,
fungi,
viruses
etc.,
various
becoming
increasingly
recognized.
microbiome
influences
neuroinflammation,
neurotransmitter
synthesis,
mitochondrial
function,
integrity
through
axis,
which
contributes
development
progression
disease.
review
delves
molecular
mechanisms
underlie
these
relationships,
emphasizing
effects
microbial
such
as
bacterial
lipopolysaccharides
(LPS),
short-chain
fatty
acids
(SCFAs)
regulating
functioning.
Additionally,
looks
at
how
environmental
dietary
decisions
whether
they
could
be
risk
factors
illnesses.
study
concludes
highlighting
critical
role
plays
It
also
provides
promising
direction
future
research
treatment
approaches.
People
afflicted
difficult
ailments
find
hope
new
preventive
therapeutic
approaches
diseases
better
understood.
Antioxidants,
Год журнала:
2025,
Номер
14(1), С. 108 - 108
Опубликована: Янв. 18, 2025
The
study
of
mitochondrial
dysfunction
has
become
increasingly
pivotal
in
elucidating
the
pathophysiology
various
cerebral
pathologies,
particularly
neurodegenerative
disorders.
Mitochondria
are
essential
for
cellular
energy
metabolism,
regulation
reactive
oxygen
species
(ROS),
calcium
homeostasis,
and
execution
apoptotic
processes.
Disruptions
function,
driven
by
factors
such
as
oxidative
stress,
excitotoxicity,
altered
ion
balance,
lead
to
neuronal
death
contribute
cognitive
impairments
several
brain
diseases.
Mitochondrial
can
arise
from
genetic
mutations,
ischemic
events,
hypoxia,
other
environmental
factors.
This
article
highlights
critical
role
progression
diseases
discusses
need
targeted
therapeutic
strategies
attenuate
damage,
restore
enhance
neuroprotection.
International Journal of Molecular Sciences,
Год журнала:
2025,
Номер
26(4), С. 1693 - 1693
Опубликована: Фев. 16, 2025
Tetraselmis
chuii
(T.
chuii)
is
a
green,
marine,
eukaryotic,
microalgae
that
was
authorized
in
the
European
Union
(EU)
as
novel
food
for
human
consumption
2014,
and
supplement
2017.
This
narrative
review
will
provide
an
overview
of
preclinical
clinical
trials
assessing
efficacy
T.
chuii-derived
ingredient,
characterized
by
high
superoxide
dismutase
(SOD)
activity
(SOD-rich
chuii),
to
improve
various
aspects
cellular
health.
Collectively,
results
from
vitro,
more
importantly
vivo
research,
support
SOD-rich
potential
promoter
Principally,
ingredient
appears
function
indirect
antioxidant
boosting
intracellular
systems.
Moreover,
it
can
positively
modulate
inflammatory
status
up-regulating
anti-inflammatory
down-regulating
pro-inflammatory
cytokines
factors.
In
addition,
promote
health
though
protecting
DNA
damage,
immune
function,
strengthening
cell
structure
integrity,
modulating
signaling
pathways.
There
also
some
evidence
suggest
may
mitochondrial
through
up-regulation
genes
linked
biogenesis
ATP
synthesis.
From
conducted
date,
transcriptional
activation
nuclear
factor
erythroid
2-related
2
(NRF2)
sirtuin
1
(SIRT1)
appear
be
important
mediating
effects
on
These
exciting
preliminary
observations
represent
natural
blue
with
enhance
Poultry Science,
Год журнала:
2023,
Номер
103(2), С. 103278 - 103278
Опубликована: Ноя. 17, 2023
It
has
been
hypothesized
that
reducing
the
bioenergetic
costs
of
gut
inflammation
as
an
explanation
for
effect
antibiotic
growth
promoters
(AGPs)
on
animal
efficiency,
framing
some
observations
but
not
explaining
increase
in
rate
or
prevention
infectious
diseases.
The
host's
ability
to
adapt
alterations
environmental
conditions
and
maintain
health
involves
managing
all
physiological
interactions
regulate
homeostasis.
Thus,
metabolic
pathways
are
vital
regulating
energetic
demands
host
guides
most
biological
functions.
Mitochondria
only
heart
cell
because
their
role
energy
metabolism
oxidative
phosphorylation,
also
a
central
hub
signal
transduction
receive
messages
about
nutritional
states
cells
tissues.
In
response,
mitochondria
direct
cellular
tissue
throughout
host.
endosymbiotic
theory
suggests
evolved
from
prokaryotes,
emphasizing
idea
these
organelles
can
be
affected
by
antibiotics.
Indeed,
therapeutic
levels
several
antibiotics
toxic
mitochondria,
subtherapeutic
may
improve
mitochondrial
function
defense
mechanisms
inducing
adaptive
response
cell,
resulting
mitokine
production
which
coordinates
array
responses
stressor(s).
This
stress
is
observed
bacteria
species,
suggesting
this
protective
mechanism
preserved
during
evolution.
Concordantly,
microbiome
modulation
sub-inhibitory
concentration
AGPs
could
result
stimulation
rather
than
inhibition
determined
microbial
species.
eukaryotes,
internal
external
conditions,
promote
organism
evolutionary
strategy
overcome
potential
negative
conditions.
We
hypothesize
indirect
AGP
regulation
functional
output
homeostatic
control
manner
similar
those
involved
with
disease
tolerance.
Heliyon,
Год журнала:
2024,
Номер
10(12), С. e32899 - e32899
Опубликована: Июнь 1, 2024
Natural
products
are
being
developed
as
possible
treatment
options
due
to
the
rising
prevalence
of
cancer
and
harmful
side
effects
synthetic
medications.
Arctiin
is
a
naturally
occurring
lignan
found
in
numerous
plants
exhibits
different
pharmacological
activities,
along
with
cancer.
To
elucidate
anticancer
properties
underlying
mechanisms
action,
comprehensive
search
various
electronic
databases
was
conducted
using
appropriate
keywords
identify
relevant
publications.
The
findings
suggest
that
arctiin
against
tumor
formation
cancers
such
cervical,
myeloma,
prostate,
endothelial,
gastric,
colon
several
preclinical
investigations.
This
compound
exerts
its
effect
through
cellular
mechanisms,
including
mitochondrial
dysfunction,
cell
cycle
at
phases
(G2/M),
inhibition
proliferation,
apoptotic
death,
cytotoxic
effects,
well
migration
invasion
malignant
cells.
Moreover,
study
also
revealed
that,
among
pathways,
shown
be
more
potent
terms
PI3K/AKT
JAK/STAT
signaling
pathways.
However,
pharmacokinetic
investigation
indicated
compound's
poor
oral
bioavailability.
Because
these
findings,
might
considered
promising
chemotherapeutic
drug
candidate.
Antioxidants,
Год журнала:
2024,
Номер
13(8), С. 906 - 906
Опубликована: Июль 26, 2024
Metabolic
dysfunction-associated
steatotic
liver
disease
(MASLD),
formerly
known
as
nonalcoholic
fatty
(NAFLD),
encompasses
a
range
of
conditions
from
steatosis
to
steatohepatitis
(NASH).
Its
prevalence,
especially
among
patients
with
metabolic
syndrome,
highlights
its
growing
global
impact.
The
pathogenesis
MASLD
involves
dysregulation,
inflammation,
oxidative
stress,
genetic
factors
and,
notably,
mitochondrial
dysfunction.
Recent
studies
underscore
the
critical
role
dysfunction
in
MASLD's
progression.
Therapeutically,
enhancing
function
has
gained
interest,
along
lifestyle
changes
and
pharmacological
interventions
targeting
processes.
FDA's
approval
resmetirom
for
metabolic-associated
(MASH)
fibrosis
marks
significant
step.
While
represents
progress,
further
research
is
essential
understand
MASLD-related
fully.
Innovative
strategies
like
gene
editing
small-molecule
modulators,
alongside
interventions,
can
potentially
improve
treatment.
Drug
repurposing
new
targets
will
advance
therapy,
addressing
increasing
burden.
Therefore,
this
review
aims
provide
better
understanding
identify
more
effective
preventive
treatment
strategies.
CNS Neuroscience & Therapeutics,
Год журнала:
2024,
Номер
30(8)
Опубликована: Авг. 1, 2024
Abstract
Synaptic
plasticity
is
believed
to
underlie
the
cellular
and
molecular
basis
of
memory
formation.
Mitochondria
are
one
main
organelles
involved
in
metabolism
energy
maintenance
as
plastic
that
change
morphologically
functionally
response
needs
regulate
synaptic
function
through
multiple
mechanisms,
including
ATP
generation,
calcium
homeostasis,
biogenesis.
An
increased
neuronal
activity
enhances
efficiency,
during
which
mitochondria's
spatial
distribution
morphology
significantly.
These
build
up
pre‐and
postsynaptic
zones
produce
ATP,
necessary
for
several
processes
like
neurotransmitter
release
recycling.
also
homeostasis
by
buffering
intracellular
calcium,
ensures
proper
activity.
Furthermore,
mitochondria
presynaptic
terminal
have
distinct
morphological
properties
compared
dendritic
or
mitochondria.
This
specialization
enables
precise
control
plasticity.
Mitochondrial
dysfunction
has
been
linked
failure
many
neurodegenerative
disorders,
Alzheimer's
disease
(AD).
In
AD,
malfunctioning
cause
delays
vesicle
recycling,
ionic
gradient
imbalances,
mostly
failure.
review
emphasizes
mitochondrial
plasticity's
contribution
function.
It
explores
profound
effect
malfunction
on
focusing
provides
an
overview
how
they
sustain
health
under
normal
conditions
their
contributes
diseases,
highlighting
potential
a
therapeutic
target
such
conditions.
Journal of Neuroinflammation,
Год журнала:
2024,
Номер
21(1)
Опубликована: Ноя. 12, 2024
Abstract
Postoperative
cognitive
dysfunction
(POCD)
is
a
frequent
neurological
complication
encountered
during
the
perioperative
period
with
unclear
mechanisms
and
no
effective
treatments.
Recent
research
into
pathogenesis
of
POCD
has
primarily
focused
on
neuroinflammation,
oxidative
stress,
changes
in
neural
synaptic
plasticity
neurotransmitter
imbalances.
Given
high-energy
metabolism
neurons
their
critical
dependency
mitochondria,
mitochondrial
directly
affects
neuronal
function.
Additionally,
as
primary
organelles
generating
reactive
oxygen
species,
mitochondria
are
closely
linked
to
pathological
processes
neuroinflammation.
Surgery
anesthesia
can
induce
dysfunction,
increase
disrupt
quality-control
via
various
pathways,
hence
serving
key
initiators
process.
We
conducted
review
role
potential
postoperative
by
consulting
relevant
literature
from
PubMed
EMBASE
databases
spanning
past
25
years.
Our
findings
indicate
that
surgery
inhibit
respiration,
thereby
reducing
ATP
production,
decreasing
membrane
potential,
promoting
fission,
inducing
calcium
buffering
abnormalities
iron
accumulation,
inhibiting
mitophagy,
increasing
stress.
Mitochondrial
damage
ultimately
lead
impaired
function,
abnormal
transmission,
synthesis
release
neurotransmitters,
even
death,
resulting
dysfunction.
Targeted
therapies
have
shown
positive
outcomes,
holding
promise
novel
treatment
for
POCD.