International Journal of Molecular Sciences,
Год журнала:
2019,
Номер
20(14), С. 3439 - 3439
Опубликована: Июль 12, 2019
Magnesium
(Mg)
is
the
second
most
abundant
cation
in
mammalian
cells,
and
it
essential
for
numerous
cellular
processes
including
enzymatic
reactions,
ion
channel
functions,
metabolic
cycles,
signaling,
DNA/RNA
stabilities.
Because
of
versatile
universal
nature
Mg2+,
homeostasis
intracellular
Mg2+
physiologically
linked
to
growth,
proliferation,
differentiation,
energy
metabolism,
death
cells.
On
tissue
levels,
maintaining
within
optimal
levels
according
biological
context,
such
as
cell
types,
developmental
stages,
extracellular
environments,
pathophysiological
conditions,
crucial
development,
normal
diseases.
Hence,
pathologically
involved
cancers,
diabetes,
neurodegenerative
diseases,
Parkinson’s
disease,
Alzheimer’s
demyelination.
In
research
field
regarding
roles
mechanisms
regulation,
controversies
caused
by
its
versatility
complexity
still
exist.
As
at
least,
plays
critical
neuronal
healthy
appropriate
supplementation
exhibits
neurotrophic
effects
a
majority
cases.
control
can
be
candidate
therapeutic
targets
this
review,
recent
results
regulatory
system
determining
phenotype,
fate,
diseases
nervous
are
summarized,
an
overview
comprehensive
provided.
Life,
Год журнала:
2024,
Номер
14(2), С. 196 - 196
Опубликована: Янв. 30, 2024
Alzheimer’s
disease
(AD)
is
a
progressive
and
incurable
neurodegenerative
disorder
that
primarily
affects
persons
aged
65
years
above.
It
causes
dementia
with
memory
loss
deterioration
in
thinking
language
skills.
AD
characterized
by
specific
pathology
resulting
from
the
accumulation
brain
of
extracellular
plaques
amyloid-β
intracellular
tangles
phosphorylated
tau.
The
importance
mitochondrial
dysfunction
pathogenesis,
while
previously
underrecognized,
now
more
appreciated.
Mitochondria
are
an
essential
organelle
involved
cellular
bioenergetics
signaling
pathways.
Mitochondrial
processes
crucial
for
synaptic
activity
such
as
mitophagy,
trafficking,
fission,
fusion
dysregulated
brain.
Excess
fission
fragmentation
yield
mitochondria
low
energy
production.
Reduced
glucose
metabolism
also
observed
hypometabolic
state,
particularly
temporo-parietal
regions.
This
review
addresses
multiple
ways
which
abnormal
structure
function
contribute
to
AD.
Disruption
electron
transport
chain
ATP
production
neurotoxic
because
cells
have
disproportionately
high
demands.
In
addition,
oxidative
stress,
extremely
damaging
nerve
cells,
rises
dramatically
dyshomeostasis.
Restoring
health
may
be
viable
approach
treatment.
Acta Pharmacologica Sinica,
Год журнала:
2024,
Номер
45(7), С. 1337 - 1348
Опубликована: Фев. 13, 2024
Abstract
Transforming
growth
factor-β
(TGF-β)
signaling
is
initiated
by
activation
of
transmembrane
TGF-β
receptors
(TGFBR),
which
deploys
Smad2/3
transcription
factors
to
control
cellular
responses.
Failure
or
dysregulation
in
the
pathways
leads
pathological
conditions.
regulated
at
different
levels
along
and
begins
with
liberation
ligand
from
its
latent
form.
The
mechanisms
TGFBR
display
selectivity
cell
types,
agonists,
isoforms,
enabling
precise
signals.
In
addition,
surface
compartments
used
release
active
are
surprisingly
vibrant,
using
thrombospondins,
integrins,
matrix
metalloproteinases
reactive
oxygen
species.
scope
further
unfolded
discovery
other
pathways.
unique
combination
works
series
trigger
activation,
can
be
explored
as
therapeutic
targets.
This
comprehensive
review
provides
valuable
insights
into
diverse
underpinning
shedding
light
on
potential
avenues
for
exploration.
Signal Transduction and Targeted Therapy,
Год журнала:
2025,
Номер
10(1)
Опубликована: Янв. 2, 2025
Abstract
Rampant
phospholipid
peroxidation
initiated
by
iron
causes
ferroptosis
unless
this
is
restrained
cellular
defences.
Ferroptosis
increasingly
implicated
in
a
host
of
diseases,
and
unlike
other
cell
death
programs
the
physiological
initiation
conceived
to
occur
not
an
endogenous
executioner,
but
withdrawal
guardians
that
otherwise
constantly
oppose
induction.
Here,
we
profile
key
ferroptotic
defence
strategies
including
regulation,
modulation
enzymes
metabolite
systems:
glutathione
reductase
(GR),
suppressor
protein
1
(FSP1),
NAD(P)H
Quinone
Dehydrogenase
(NQO1),
Dihydrofolate
(DHFR),
retinal
reductases
dehydrogenases
(RDH)
thioredoxin
(TR).
A
common
thread
uniting
all
metabolites
combat
lipid
during
dependence
on
reductant,
nicotinamide
adenine
dinucleotide
phosphate
(NADPH).
We
will
outline
how
cells
control
central
carbon
metabolism
produce
NADPH
necessary
precursors
defend
against
ferroptosis.
Subsequently
discuss
evidence
for
dysregulation
different
disease
contexts
glucose-6-phosphate
dehydrogenase
deficiency,
cancer
neurodegeneration.
Finally,
several
anti-ferroptosis
therapeutic
spanning
use
radical
trapping
agents,
dependent
redox
support
highlight
current
landscape
clinical
trials
focusing
Oxidative Medicine and Cellular Longevity,
Год журнала:
2020,
Номер
2020, С. 1 - 27
Опубликована: Июль 3, 2020
The
blood-brain
barrier
(BBB),
as
a
crucial
gate
of
brain-blood
molecular
exchange,
is
involved
in
the
pathogenesis
multiple
neurological
diseases.
Oxidative
stress
caused
by
an
imbalance
between
production
reactive
oxygen
species
(ROS)
and
scavenger
system.
Since
oxidative
plays
significant
role
maintenance
BBB,
cerebrovascular
system
especially
vulnerable
to
it.
pathways
that
initiate
BBB
dysfunction
include,
but
are
not
limited
to,
mitochondrial
dysfunction,
excitotoxicity,
iron
metabolism,
cytokines,
pyroptosis,
necroptosis,
all
converging
on
generation
ROS.
Interestingly,
ROS
also
provide
common
triggers
directly
regulate
damage,
parameters
including
tight
junction
(TJ)
modifications,
transporters,
matrix
metalloproteinase
(MMP)
activation,
inflammatory
responses,
autophagy.
We
will
discuss
stress-mediated
disruption
diseases,
such
hemorrhagic
stroke,
ischemic
stroke
(IS),
Alzheimer’s
disease
(AD),
Parkinson’s
(PD),
traumatic
brain
injury
(TBI),
amyotrophic
lateral
sclerosis
(ALS),
cerebral
small
vessel
(CSVD).
This
review
latest
clinical
evidence
potential
biomarkers
antioxidant
drugs
towards
A
deeper
understanding
how
damages
may
open
up
more
therapeutic
options
for
treatment
International Journal of Molecular Sciences,
Год журнала:
2019,
Номер
20(14), С. 3439 - 3439
Опубликована: Июль 12, 2019
Magnesium
(Mg)
is
the
second
most
abundant
cation
in
mammalian
cells,
and
it
essential
for
numerous
cellular
processes
including
enzymatic
reactions,
ion
channel
functions,
metabolic
cycles,
signaling,
DNA/RNA
stabilities.
Because
of
versatile
universal
nature
Mg2+,
homeostasis
intracellular
Mg2+
physiologically
linked
to
growth,
proliferation,
differentiation,
energy
metabolism,
death
cells.
On
tissue
levels,
maintaining
within
optimal
levels
according
biological
context,
such
as
cell
types,
developmental
stages,
extracellular
environments,
pathophysiological
conditions,
crucial
development,
normal
diseases.
Hence,
pathologically
involved
cancers,
diabetes,
neurodegenerative
diseases,
Parkinson’s
disease,
Alzheimer’s
demyelination.
In
research
field
regarding
roles
mechanisms
regulation,
controversies
caused
by
its
versatility
complexity
still
exist.
As
at
least,
plays
critical
neuronal
healthy
appropriate
supplementation
exhibits
neurotrophic
effects
a
majority
cases.
control
can
be
candidate
therapeutic
targets
this
review,
recent
results
regulatory
system
determining
phenotype,
fate,
diseases
nervous
are
summarized,
an
overview
comprehensive
provided.
