Frontiers in Cell and Developmental Biology,
Journal Year:
2024,
Volume and Issue:
12
Published: Nov. 19, 2024
Sciences
(IUCS-CESPU),
4585-116
Gandra,
Portugal.
*Correspondence:
Patrícia
M.
A.
Silva
([email protected])The
balanced
regulation
of
cell
death
and
survival
is
critical
for
maintaining
the
homeostasis
human
body.
Disruption
this
delicate
equilibrium
often
underlies
development
several
diseases.
For
instance,
cancer
cells
develop
resistance
to
natural
mechanisms,
leading
uncontrolled
proliferation
malignant
growth
(1,2).
Conversely,
neurodegenerative
diseases
involve
progressive
loss
specific
brain
populations,
resulting
in
a
broad
spectrum
debilitating
symptoms
and,
ultimately,
(3,
4)
(Figure
1).The
incidence
prevalence
both
are
rising
rapidly,
significantly
impacting
patients'
quality
life
creating
major
economic
healthcare
challenges
worldwide
(5,6).
While
knowledge
about
role
abnormal
these
has
advanced,
precise
mechanisms
driving
processes,
as
well
effective
strategies
modulate
them,
remain
only
partially
understood.
This
limited
understanding
complicates
efforts
tailor
treatments
different
disease
types.
cancer,
therapeutic
approaches
focus
on
inducing
eliminate
cells,
whereas
diseases,
goal
shifts
preventing
preserve
affected
neurons
delay
symptom
progression.
Research
Topic
focused
enriching
our
emerging
modulators
death,
exploring
their
action
potential
applications
various
scenarios.In
total,
two
original
research
articles
three
review
were
published.
editorial
briefly
summarizes
findings
highlights
key
insights
derived
from
articles,
emphasizing
contributions
field
they
present
guiding
future
and/or
strategies.
release
ALL
dependent
Gαi
subunit,
its
inhibition
blocks
process
without
affecting
Gβϒ.
Moreover,
further
experiments
showed
that
activating
adenylyl
cyclase
(AC)
with
forskolin
or
using
8-CPT-cAMP
inhibits
D,L-methadone-induced
ER
Ca
2+
release,
suggesting
Gαi-mediated
downregulation
AC
cAMP.
Notably,
protein
kinase
A
(PKA)
inhibitor
14-22
amide
(myr)
can
independently
elicit
Metabolites,
Journal Year:
2025,
Volume and Issue:
15(2), P. 124 - 124
Published: Feb. 13, 2025
Neurodegenerative
diseases
comprise
a
group
of
chronic,
usually
age-related,
disorders
characterized
by
progressive
neuronal
loss,
deformation
structure,
or
loss
function,
leading
to
substantially
reduced
quality
life.
They
remain
significant
focus
scientific
and
clinical
interest
due
their
increasing
medical
social
importance.
Most
neurodegenerative
present
intracellular
protein
aggregation
extracellular
deposition
(plaques),
such
as
α-synuclein
in
Parkinson's
disease
amyloid
beta
(Aβ)/tau
aggregates
Alzheimer's.
Conventional
treatments
for
conditions
incur
high
costs
are
related
the
development
several
adverse
effects.
In
addition,
many
patients
irresponsive
them.
For
these
reasons,
there
is
growing
tendency
find
new
therapeutic
approaches
help
patients.
This
review
intends
investigate
some
phytocompounds'
effects
on
diseases.
These
generally
increased
oxidative
stress
inflammation,
so
phytocompounds
can
prevent
treat
To
achieve
our
aim
provide
critical
assessment
current
literature
about
phytochemicals
targeting
neurodegeneration,
we
reviewed
reputable
databases,
including
PubMed,
EMBASE,
COCHRANE,
seeking
trials
that
utilized
against
conditions.
A
few
investigated
humans,
after
screening,
13
were
ultimately
included
following
PRISMA
guidelines.
compounds
include
polyphenols
(flavonoids
luteolin
quercetin,
phenolic
acids
rosmarinic
acid,
ferulic
caffeic
other
like
resveratrol),
alkaloids
(such
berberine,
huperzine
A,
caffeine),
terpenoids
ginkgolides
limonene).
The
gathered
evidence
underscores
caffeine,
ginkgolides,
primarily
anti-inflammatory,
antioxidant,
neuroprotective,
counteracting
neuroinflammation,
oxidation,
synaptic
dysfunctions,
which
crucial
aspects
intervention
various
conditions,
Alzheimer's
dementias,
depression,
neuropsychiatric
disorders.
summary,
they
show
use
improvements
cognition,
memory,
disinhibition,
irritability/lability,
aberrant
behavior,
hallucinations,
mood
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(3), P. 1019 - 1019
Published: Jan. 25, 2025
Atherosclerosis
is
a
complex
inflammatory
process
associated
with
high-mortality
cardiovascular
diseases.
Today,
there
growing
body
of
evidence
linking
atherosclerosis
to
mutations
mitochondrial
DNA
(mtDNA).
But
the
mechanism
this
link
insufficiently
studied.
progression
involves
different
cell
types
and
macrophages
are
one
most
important.
Due
their
high
plasticity,
can
demonstrate
pro-inflammatory
pro-atherogenic
(macrophage
type
M1)
or
anti-inflammatory
anti-atherogenic
M2)
effects.
These
two
types,
formed
as
result
external
stimuli,
differ
significantly
in
metabolic
profile,
which
suggests
central
role
mitochondria
implementation
macrophage
polarization
route.
According
this,
we
assume
that
mtDNA
causing
disturbances
play
an
internal
trigger,
leading
formation
M1
M2.
This
review
provides
comparative
analysis
characteristics
function
possible
associations
linked
inflammation-based
pathologies
including
atherosclerosis.
Biochemical Society Transactions,
Journal Year:
2024,
Volume and Issue:
52(4), P. 1939 - 1946
Published: Aug. 22, 2024
Intracellular
communication
and
regulation
in
brain
cells
is
controlled
by
the
ubiquitous
Ca2+
redox
signalling.
Both
of
these
independent
signalling
systems
regulate
most
processes
including
cell
surviving
mechanism
or
death.
In
physiology
can
trigger
reactive
oxygen
species
(ROS)
production
various
enzymes
mitochondria
but
ROS
could
also
transmit
signal
to
calcium
levels
via
modification
channels
phospholipase
activity.
Changes
lead
severe
pathology
resulting
excitotoxicity
oxidative
stress.
Interaction
essential
opening
mitochondrial
permeability
transition
pore
-
initial
step
apoptosis,
ROS-induced
stress
involved
necrosis
ferroptosis.
Here
we
review
role
cytosol
neurons
astrocytes
how
this
integration
pathology,
ischaemia
injury
neurodegeneration.
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
15
Published: Sept. 5, 2024
Epilepsy,
a
complex
neurological
condition
marked
by
recurring
seizures,
is
increasingly
recognized
for
its
intricate
relationship
with
mitochondria,
the
cellular
powerhouses
responsible
energy
production
and
calcium
regulation.
This
review
offers
an
in-depth
examination
of
interplay
between
epilepsy,
mitochondrial
function,
aging.
Many
factors
might
account
correlation
epilepsy
Mitochondria,
integral
to
dynamics
neuronal
excitability,
perform
critical
role
in
pathophysiology
epilepsy.
The
mechanisms
linking
mitochondria
are
multifaceted,
involving
dysfunction,
reactive
oxygen
species
(ROS),
dynamics.
Mitochondrial
dysfunction
can
trigger
seizures
compromising
ATP
production,
increasing
glutamate
release,
altering
ion
channel
function.
ROS,
natural
byproducts
respiration,
contribute
oxidative
stress
neuroinflammation,
epileptogenesis.
govern
fusion
fission
processes,
influence
seizure
threshold
buffering,
impact
propagation.
Energy
demands
during
highlight
generation
maintaining
membrane
potential.
handling
dynamically
modulates
affecting
synaptic
transmission
action
potential
generation.
Dysregulated
hallmark
contributing
excitotoxicity.
Epigenetic
modifications
function
through
histone
modifications,
DNA
methylation,
non-coding
RNA
expression.
Potential
therapeutic
avenues
targeting
include
mitochondria-targeted
antioxidants,
ketogenic
diets,
metabolic
therapies.
concludes
outlining
future
directions
research,
emphasizing
integrative
approaches,
advancements
ethical
considerations.
Mitochondria
emerge
as
central
players
narrative
offering
profound
insights
this
challenging
disorder.
Journal of Cellular Physiology,
Journal Year:
2025,
Volume and Issue:
240(1)
Published: Jan. 1, 2025
Programmed
cell
death
(apoptosis)
is
essential
part
of
the
process
tissue
regeneration
that
also
plays
role
in
mechanism
pathology.
The
phenomenon
fast
and
transient
permeability
mitochondrial
membranes
by
various
triggers,
known
as
transition
pore
(mPTP)
leads
to
release
proapoptotic
proteins
acts
an
initial
step
initiation
apoptosis.
However,
a
for
mPTP
was
suggested
physiology
it
unclear
if
there
threshold
number
mitochondria
with
which
induces
how
this
regulated
different
tissues.
Using
simultaneous
measurements
membrane
potential
fluorescent
marker
caspase-3
activation
we
studied
calcium-induced
opening
necessary
induction
apoptosis
rat
primary
cortical
neurons,
astrocytes,
fibroblasts,
cancer
(BT-474)
cells.
correlated
80%-90%
signal
loss
neural
cells
but
only
35%
BT-474
over
90%
opens
before
becomes
obvious.
induce
did
not
correlate
total
expression
levels
consistent
Bax/Bcl-2
ratio
these
Calcium-induced
increased
necrosis
higher
fibroblasts
compared
astrocytes
Thus,
tissues
require
specific
numbers
PTP
correlates
proapoptotic/antiapoptotic
them.
Cells,
Journal Year:
2025,
Volume and Issue:
14(3), P. 206 - 206
Published: Jan. 30, 2025
Multiple
sclerosis
(MS)
is
an
inflammatory
autoimmune
disease
of
the
central
nervous
system
(CNS)
linked
to
many
neurological
disabilities.
The
visual
frequently
impaired
in
MS.
In
previous
studies,
we
observed
early
malfunctions
rod
photoreceptor
ribbon
synapses
EAE
mouse
model
MS
that
included
alterations
synaptic
vesicle
cycling
and
disturbances
presynaptic
Ca2+
homeostasis.
Since
these
events
are
highly
energy-demanding,
analyzed
whether
mitochondria,
which
play
a
major
role
energy
metabolism,
might
be
involved
at
stage.
Rod
terminals
contain
single
large
mitochondrion
next
ribbon.
present
study,
expression
functionally
relevant
mitochondrial
proteins
(MIC60,
ATP5B,
COX1,
PINK1,
DRP1)
by
high-resolution
qualitative
quantitative
immunofluorescence
microscopy,
immunogold
electron
microscopy
Western
blot
experiments.
We
decreased
mitochondria
photoreceptors
stage,
suggesting
dysfunctions
important
synapse
pathology.
Interestingly,
were
strongly
compromised
EAE,
whereas
extra-synaptic
inner
segments
remained
unchanged,
demonstrating
functional
heterogeneity
mitochondria.
Frontiers in Bioscience-Landmark,
Journal Year:
2025,
Volume and Issue:
30(3)
Published: March 18, 2025
Background:
Amyotrophic
lateral
sclerosis
(ALS)
is
a
progressive
multisystem
disease
characterized
by
limb
and
trunk
muscle
weakness
that
attributed,
in
part,
to
abnormalities
mitochondrial
ultrastructure
impaired
functions.
This
study
investigated
the
time
course
of
structural
functional
rearrangements
skeletal
mitochondria
combination
with
motor
impairments
Tg
(copper-zinc
superoxide
dismutase
enzyme
(SOD1)
G93A)
dl1/GurJ
(referred
as
SOD1-G93A/low)
male
mice,
familial
ALS
model,
compared
non-transgenic
littermates.
Methods:
The
neurological
status
functions
were
assessed
weekly
using
paw
grip
endurance
method
grid
suspension
test
two-limb
four-limb
tasks.
Transmission
electron
microscopy
followed
quantitative
analysis
was
performed
ultrastructural
alterations
quadriceps
femoris.
Functional
high-resolution
Oxygraph-2k
(O2K)
respirometry
methods
for
assessing
calcium
retention
capacity
index
content
lipid
peroxidation
products
freshly
isolated
preparations.
Results:
Based
on
behavioral
phenotyping
data,
specific
age
groups
identified:
postnatal
day
56
(P56)
(n
=
10–11),
84
(P84)
156
(P154)
10–12),
representing
pre-symptomatic,
early-symptomatic
late-symptomatic
stages
progression
SOD1-G93A/low
respectively.
Electron
showed
mosaic
destructive
changes
subsarcolemmal
fibers
femoris
from
84-day-old
mice.
Morphometric
revealed
an
elevation
mean
size
SOD1-G93A
mice
at
P84
P154.
In
addition,
P154
transgenic
group
demonstrated
decrease
sarcomere
width
number
per
unit
area.
At
symptomatic
stage,
exhibited
decreased
respiratory
control
ratio,
ADP-stimulated,
uncoupled
respiration
rates
muscle,
measured
respirometry.
parallel,
lower
increased
levels
control.
Conclusions:
Taken
together,
these
results
indicate
stage-dependent
associated
defective
oxidative
phosphorylation,
homeostasis,
damage
mouse
which
appears
be
promising
direction
development
therapies
ALS.