Frontiers in Cell and Developmental Biology,
Journal Year:
2025,
Volume and Issue:
12
Published: Jan. 6, 2025
Graves
disease
(GD),
an
autoimmune
affects
the
thyroid
gland,
results
in
hyperthyroidisms
and
goiter.
The
main
cause
of
GD
is
not
clearly
defined;
however,
stimulating
autoantibodies
for
hormone
receptor
(TSHR)
known
as
thyroid-stimulating
immunoglobulins
(TSIs)
are
primary
proposed
mechanism.
TSI
activation
TSHRs
gland
excessive
release
hormones
with
subsequent
development
hyperthyroidism
cellular
process
macroautophagy/autophagy
implicated
pathogenesis
other
diseases.
Autophagy
plays
a
critical
role
many
diseases
different
stages
same
through
modulation
immunity
inflammatory
response.
In
addition,
autophagy
also
thyroid-associated
ophthalmopathy
(TAO).
However,
exact
well
explained.
Therefore,
this
review
discusses
how
intricately
involved
regarding
its
protective
harmful
effects.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(8), P. 4161 - 4161
Published: April 9, 2024
Neuroinflammation
and
epilepsy
are
different
pathologies,
but,
in
some
cases,
they
so
closely
related
that
the
activation
of
one
pathologies
leads
to
development
other.
In
this
work,
we
discuss
three
main
cell
types
involved
neuroinflammation,
namely
(i)
reactive
astrocytes,
(ii)
activated
microglia,
infiltration
(iii)
peripheral
immune
cells
central
nervous
system.
Then,
how
neuroinflammation
interconnected
describe
use
repurposing
drugs
with
anti-inflammatory
properties
have
been
shown
a
beneficial
effect
models.
This
review
reinforces
idea
compounds
designed
alleviate
seizures
need
target
not
only
caused
by
astrocytes
microglia
but
also
interaction
these
infiltrated
cells.
Diabetes Obesity and Metabolism,
Journal Year:
2024,
Volume and Issue:
26(8), P. 3031 - 3044
Published: May 27, 2024
Abstract
Depression
is
a
mood
disorder
that
may
increase
risk
for
the
development
of
insulin
resistance
(IR)
and
type
2
diabetes
(T2D),
vice
versa.
However,
mechanistic
pathway
linking
depression
T2D
not
fully
elucidated.
The
aim
this
narrative
review,
therefore,
was
to
discuss
possible
link
between
T2D.
coexistence
twice
as
great
compared
occurrence
either
condition
independently.
Hyperglycaemia
dyslipidaemia
promote
incidence
by
enhancing
inflammation
reducing
brain
serotonin
(5‐hydroxytryptamine
[5HT]).
Dysregulation
signalling
in
impairs
5HT
signalling,
leading
depression.
Furthermore,
associated
with
hyperglycaemia
poor
glycaemic
control.
Psychological
stress
In
conclusion,
could
be
potential
factor
through
induction
inflammatory
reactions
oxidative
affect
neurotransmission.
addition,
chronic
induce
dysregulation
hypothalamic–pituitary–adrenal
axis
circulating
cortisol
levels,
which
triggers
IR
Brain Research Bulletin,
Journal Year:
2025,
Volume and Issue:
221, P. 111189 - 111189
Published: Jan. 5, 2025
Epilepsy
is
a
neurological
disease
characterized
by
unprovoked
recurrent
epileptic
seizures.
Temporal
lobe
epilepsy
(TLE)
the
commonest
type
of
focal
in
adults
that
resist
to
conventional
anti-seizure
medications
(ASMs).
Interestingly,
ASMs
do
not
affect
epileptogenesis
and
progression
disease.
Therefore,
repurposing
natural
products
with
anti-inflammatory,
anti-oxidant
effects
such
as
berberine
(BRB)
may
be
logical
treating
refractory
TLE.
However,
molecular
mechanism
BRB
against
development
seizure
mainly
TLE
was
fully
elucidated.
we
attempt
this
review
discuss
potential
underlying
Autophagy,
Journal Year:
2024,
Volume and Issue:
unknown, P. 1 - 12
Published: June 14, 2024
Macroautophagy/autophagy
is
an
essential
degradation
process
that
removes
abnormal
cellular
components,
maintains
homeostasis
within
cells,
and
provides
nutrition
during
starvation.
Activated
autophagy
enhances
cell
survival
stressful
conditions,
although
overactivation
of
triggers
induction
autophagic
death.
Therefore,
early-onset
promotes
whereas
late-onset
provokes
programmed
death,
which
can
prevent
disease
progression.
Moreover,
regulates
pancreatic
β-cell
functions
by
different
mechanisms,
the
precise
role
in
type
2
diabetes
(T2D)
not
completely
understood.
Consequently,
this
mini-review
discusses
protective
harmful
roles
β
pathophysiology
T2D.
Cells,
Journal Year:
2023,
Volume and Issue:
12(22), P. 2595 - 2595
Published: Nov. 9, 2023
Metabolic
disorders
and
diabetes
(DM)
impact
more
than
five
hundred
million
individuals
throughout
the
world
are
insidious
in
onset,
chronic
nature,
yield
significant
disability
death.
Current
therapies
that
address
nutritional
status,
weight
management,
pharmacological
options
may
delay
but
cannot
alter
disease
course
or
functional
organ
loss,
such
as
dementia
degeneration
of
systemic
bodily
functions.
Underlying
these
challenges
onset
aging
associated
with
increased
lifespan,
telomere
dysfunction,
oxidative
stress
generation
lead
to
multi-system
dysfunction.
These
hurdles
point
urgent
need
underlying
mechanisms
innovative
applications.
New
treatment
strategies
involve
non-coding
RNA
pathways
microRNAs
(miRNAs)
circular
ribonucleic
acids
(circRNAs),
Wnt
signaling,
Wnt1
inducible
signaling
pathway
protein
1
(WISP1)
dependent
upon
programmed
cell
death
pathways,
cellular
metabolic
AMP-activated
kinase
(AMPK)
nicotinamide,
growth
factor
Non-coding
RNAs,
AMPK
cornerstone
for
overseeing
complex
offer
avenues
DM
will
necessitate
continued
appreciation
ability
each
independently
unison
influence
clinical
outcome.
Frontiers in Cellular Neuroscience,
Journal Year:
2025,
Volume and Issue:
18
Published: Jan. 14, 2025
Protein
lactylation
is
a
new
form
of
post-translational
modification
that
has
recently
been
proposed.
Lactoyl
groups,
derived
mainly
from
the
glycolytic
product
lactate,
have
linked
to
protein
in
brain
tissue,
which
shown
correlate
with
increased
neuronal
excitability.
Ischemic
stroke
may
promote
glycolysis,
leading
lactate
accumulation
tissue.
This
heighten
excitability
by
upregulating
levels,
potentially
triggering
post-stroke
epilepsy.
Although
current
clinical
treatments
for
seizures
advanced
significantly,
approximately
30%
patients
epilepsy
remain
unresponsive
medication,
and
prevalence
continues
rise.
study
explores
mechanisms
epilepsy-associated
death
mediated
metabolism
lactylation.
also
examines
potential
histone
deacetylase
inhibitors
alleviate
modifying
thereby
offering
fresh
perspectives
future
research
into
pathogenesis
treatment
