Antioxidants,
Journal Year:
2025,
Volume and Issue:
14(1), P. 108 - 108
Published: Jan. 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.
Cell Death Discovery,
Journal Year:
2025,
Volume and Issue:
11(1)
Published: Jan. 24, 2025
Abstract
Free
radicals,
characterized
by
the
presence
of
unpaired
electrons,
are
highly
reactive
species
that
play
a
significant
role
in
human
health.
These
molecules
can
be
generated
through
various
endogenous
processes,
such
as
mitochondrial
respiration
and
immune
cell
activation,
well
exogenous
sources,
including
radiation,
pollution,
smoking.
While
free
radicals
essential
for
certain
physiological
signaling
defense,
their
overproduction
disrupt
delicate
balance
between
oxidants
antioxidants,
leading
to
oxidative
stress.
Oxidative
stress
results
damage
critical
biomolecules
like
DNA,
proteins,
lipids,
contributing
pathogenesis
diseases.
Chronic
conditions
cancer,
cardiovascular
diseases,
neurodegenerative
disorders,
inflammatory
diseases
have
been
strongly
associated
with
harmful
effects
radicals.
This
review
provides
comprehensive
overview
characteristics
types
mechanisms
formation,
biological
impacts.
Additionally,
we
explore
natural
compounds
extracts
studied
antioxidant
properties,
offering
potential
therapeutic
avenues
managing
radical-induced
damage.
Future
research
directions
also
discussed
advance
our
understanding
treatment
radical-associated
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(17), P. 9540 - 9540
Published: Aug. 23, 2022
Alzheimer’s
disease
(AD)
is
the
most
common
age-related
dementia.
The
alteration
in
metabolic
characteristics
determines
prognosis.
Patients
at
risk
show
reduced
glucose
uptake
brain.
Additionally,
type
2
diabetes
mellitus
increases
of
AD
with
increasing
age.
Therefore,
changes
cerebral
cortex
may
predict
histopathological
diagnosis
AD.
shifts
and
metabolism,
insulin
resistance,
oxidative
stress,
abnormal
autophagy
advance
pathogenesis
syndrome.
Here,
we
summarize
role
altered
metabolism
for
discuss
potential
pharmacological
interventions
defects
to
encourage
development
novel
therapeutic
methods.
Scientific Reports,
Journal Year:
2023,
Volume and Issue:
13(1)
Published: March 6, 2023
Alzheimer's
disease
(AD)
is
a
progressive
neurodegenerative
characterized
by
the
formation
of
amyloid
plaques
implicated
in
neuronal
death.
Genetics,
age,
and
sex
are
risk
factors
attributed
to
AD.
Though
omics
studies
have
helped
identify
pathways
associated
with
AD,
an
integrated
systems
analysis
available
data
could
help
understand
mechanisms,
potential
biomarkers,
therapeutic
targets.
Analysis
transcriptomic
sets
from
GEO
database,
proteomic
metabolomic
literature
was
performed
deregulated
commonality
identified
overlapping
among
sets.
The
included
those
neurotransmitter
synapses,
oxidative
stress,
inflammation,
vitamins,
complement,
coagulation
pathways.
Cell
type
showed
microglia,
endothelial,
myeloid,
lymphoid
cells
affected.
Microglia
inflammation
pruning
synapses
implications
for
memory
cognition.
protein-cofactor
network
B2,
B6,
pantothenate
shows
metabolic
modulated
these
vitamins
which
overlap
multi-omics
analysis.
Overall,
molecular
signature
Treatment
anti-oxidants,
genetically
susceptible
individuals
pre-symptomatic
stage
might
better
management
disease.
International Journal of Molecular Medicine,
Journal Year:
2024,
Volume and Issue:
53(5)
Published: April 2, 2024
Chronic
neuroinflammation
serves
a
key
role
in
the
onset
and
progression
of
neurodegenerative
disorders.
Mitochondria
serve
as
central
regulators
neuroinflammation.
In
addition
to
providing
energy
cells,
mitochondria
also
participate
immunoinflammatory
response
disorders
including
Alzheimer's
disease,
Parkinson's
multiple
sclerosis
epilepsy,
by
regulating
processes
such
cell
death
inflammasome
activation.
Under
inflammatory
conditions,
mitochondrial
oxidative
stress,
epigenetics,
dynamics
calcium
homeostasis
imbalance
may
underlying
regulatory
mechanisms
for
these
diseases.
Therefore,
investigating
related
dysfunction
result
therapeutic
strategies
against
chronic
neurodegeneration.
The
present
review
summarizes
neuroinflammatory
diseases
current
treatment
approaches
that
target
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(9), P. 4703 - 4703
Published: April 26, 2024
Autoimmune
thyroid
disease
(AITD)
is
the
most
common
organic
specific
illness
of
gland.
It
may
manifest
as
overproduction
or
decline
thyroxine
and
triiodothyronine.
Hyperthyroidism
develops
due
to
hormones
an
answer
presence
stimulatory
antibodies
against
TSH
receptor.
Hashimoto’s
thyroiditis
(HT)
generally
characterized
by
peroxidase
thyroglobulin
antibodies,
with
a
concomitant
infiltration
lymphocytes
in
thyroid.
Due
progressive
destruction
cells,
AITD
can
lead
subclinical
overt
hypothyroidism.
Pathophysiology
extremely
complicated
still
not
fully
understood,
genetic,
environmental
epigenetic
factors
involved
its
development.
increasing
incidence
social
awareness
this
pathology,
there
urgent
need
expand
background
concerning
AITD.
A
growing
body
evidence
suggests
possible
ways
treatment
apart
from
traditional
approaches.
Simultaneously,
role
potential
new
biomarkers
diagnosis
monitoring
has
been
highlighted
recently,
too.
Therefore,
we
decided
review
therapeutic
trends
course
based
on
pathophysiological
mechanisms,
mainly
focusing
HT.
Another
aim
was
summarize
state
knowledge
regarding
condition.
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(8), P. 906 - 906
Published: July 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.
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(6), P. 687 - 687
Published: June 3, 2024
Affecting
millions
of
people
worldwide,
chronic
kidney
disease
is
a
serious
medical
problem.
It
results
in
decrease
glomerular
filtration
rate
below
60
mL/min/1.73
m,
albuminuria,
abnormalities
urine
sediment
and
pathologies
detected
by
imaging
studies
lasting
minimum
3
months.
Patients
with
CKD
develop
uremia,
as
result
the
accumulation
uremic
toxins
body,
patients
can
be
expected
to
suffer
from
number
consequences
such
progression
renal
fibrosis,
development
atherosclerosis
or
increased
incidence
cardiovascular
events.
Another
key
element
pathogenesis
oxidative
stress,
resulting
an
imbalance
between
production
antioxidants
reactive
oxygen
species.
Oxidative
stress
contributes
damage
cellular
proteins,
lipids
DNA
increases
inflammation,
perpetuating
dysfunction.
Additionally,
fibrogenesis
involving
fibrous
tissue
kidneys
occurs.
In
our
review,
we
also
included
examples
forms
therapy
for
CKD.
To
improve
condition
patients,
pharmacotherapy
used,
described
review.
Among
drugs
that
prognosis
CKD,
include:
GLP-1
analogues,
SGLT2
inhibitors,
Finerenone
monoclonal
antibody—Canakinumab
Sacubitril/Valsartan.
Biomedicine & Pharmacotherapy,
Journal Year:
2024,
Volume and Issue:
175, P. 116673 - 116673
Published: May 6, 2024
Multiple
sclerosis
(MS)
is
a
complex
autoimmune
disorder
that
impacts
the
central
nervous
system
(CNS),
resulting
in
inflammation,
demyelination,
and
neurodegeneration.
The
NOD-like
receptor
(NLR)
family
pyrin
domain-containing
3
(NLRP3)
inflammasome,
multiprotein
of
innate
immune
system,
serves
an
essential
role
pathogenesis
MS
by
regulating
production
pro-inflammatory
cytokines
(IL-1β
&
IL-18)
induction
pyroptotic
cell
death.
Mitochondrial
dysfunction
one
main
potential
factors
can
trigger
NLRP3
inflammasome
activation
lead
to
inflammation
axonal
damage
MS.
This
highlights
importance
understanding
how
mitochondrial
dynamics
modulate
activity
contribute
inflammatory
neurodegenerative
features
lack
comprehensive
urge
for
introduction
new
therapeutic
strategies
led
us
review
targeting
interplay
between
paper
also
evaluates
natural
synthetic
compounds
improve
function
and/or
inhibit
thereby
providing
neuroprotection.
Moreover,
it
summarizes
evidence
from
animal
models
demonstrate
beneficial
effects
these
on
reducing
Finally,
this
advocates
deeper
investigation
into
molecular
crosstalk
as
means
refine
targets