Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
15
Published: July 25, 2024
The
average
lifespan
of
humans
has
been
increasing,
resulting
in
a
rapidly
rising
percentage
older
individuals
and
high
morbidity
aging-associated
diseases,
especially
cardiovascular
diseases
(CVDs).
Diverse
intracellular
extracellular
factors
that
interrupt
homeostatic
functions
the
endoplasmic
reticulum
(ER)
induce
ER
stress.
Cells
employ
dynamic
signaling
pathway
unfolded
protein
response
(UPR)
to
buffer
Recent
studies
have
demonstrated
stress
triggers
various
cellular
processes
associated
with
aging
many
including
CVDs.
Autophagy
is
conserved
process
involving
lysosomal
degradation
recycling
cytoplasmic
components,
proteins,
organelles,
pathogens
invade
cytoplasm.
vital
for
combating
adverse
influence
on
heart.
present
report
summarizes
recent
mechanism
autophagy
their
overlap
CVD
pathogenesis
context
aging.
It
also
discusses
possible
therapeutic
interventions
targeting
might
delay
prevent
or
treat
Biology Direct,
Journal Year:
2025,
Volume and Issue:
20(1)
Published: March 31, 2025
Coeliac
disease
is
an
autoimmune
that
primarily
associated
with
chronic
inflammation
of
the
gut,
but
can
also
affect
organs
outside
from
liver
to
skin
and
CNS.
The
triggered
in
predisposed
individuals
by
a
peptide
mixture
(PT)
derived
digestion
gliadin,
component
wheat,
which
ingested
food.
Although
induction
endoplasmic
reticulum
stress
intestinal
epithelial
cells
(IECs)
upon
exposure
PT
known,
underlying
molecular
mechanisms
remain
unclear.
Identifying
key
players
this
signaling
pathway
could
therefore
help
develop
new
effective
therapeutic
strategy
for
treatment
CD
patients.
Two
models
were
used
identify
mechanism
linking
extracellular
(ER)
IECs
exposed
gliadin.
These
vitro
model
based
on
CaCo-2
ex
vivo
our
previously
described
gut
system
(GEVS),
both
PT.
Our
results
clearly
show
interaction
gliadin
peptides
transmembrane
CXCR3
receptor
leads
rapid
PLC
activity
generates
IP3
molecules.
This
second
messenger
binds
IP3R
located
ER
membranes,
resulting
calcium
efflux
organelle.
PT-dependent
observed
patients
excessive
release
ER.
Importantly,
inhibition
abrogates
stress,
turn
attenuates
downstream
signs
CD,
such
as
TG2
expression
permeability
dysregulation,
well
inhibits
inflammation.
Alzheimer s & Dementia,
Journal Year:
2025,
Volume and Issue:
21(4)
Published: April 1, 2025
Abstract
INTRODUCTION
This
study
examined
the
effects
of
long‐term
cervical
lymphadenectomy
(cLE)
on
cognitive
and
Alzheimer's
disease
(AD)–like
tauopathy
changes.
METHODS
Male
C57BL/6
mice
were
used
to
assess
cLE
impacts
sleep,
brain
pathways,
pathologies.
RNA
sequencing
proteomics
analyzed
gene/protein
changes,
with
results
verified
by
western
blotting
immunofluorescence.
RESULTS
CLE
led
sleep
psychiatric
disorders,
linked
mitogen‐activated
protein
kinase/extracellular
signal‐regulated
kinase
(ERK)
pathway
activation.
Activation
ERK
may
interfere
autophagy
is
associated
phosphorylated
tau
accumulation.
Peripheral
blood
analysis
shows
decreased
waste
in
peripheral
post‐cLE,
implicating
impaired
lymphatic
drainage
build‐up.
DISCUSSION
These
findings
suggest
a
potential
connection
between
AD‐like
tauopathy,
potentially
influencing
surgical
decisions.
Highlights
Cervical
cornerstone
head
neck
cancers,
affecting
millions
people
each
year.
We
provide
first
evidence
mildly
functioning
significant
anxiety–depressive
disorders
after
cLE.
Long‐term
not
only
directly
impairs
wastes
(amyloid
beta,
[p‐tau])
drainage,
but
also
activates
Erk1/2
signaling
leading
attenuation
autophagy.
found
for
time
that
accelerated
deposition
p‐tau
young
mice.
Patients
clinical
lymph
node
dissection
showed
reduced
consistent
mouse
models.
suggests
need
further
evaluation
neurologic
dissection,
procedure
affects
Stresses,
Journal Year:
2025,
Volume and Issue:
5(2), P. 26 - 26
Published: April 4, 2025
Cellular
stressors
have
been
demonstrated
to
exert
a
substantial
influence
on
the
functionality
of
organelles,
thereby
impacting
cellular
homeostasis
and
contributing
development
disease
pathogenesis.
This
review
aims
examine
impact
diverse
stressors,
including
environmental,
chemical,
biological,
physical
factors,
critical
organelles
such
as
cell
membrane,
mitochondria,
endoplasmic
reticulum,
Golgi
apparatus,
lysosomes,
membrane-less
organelles.
The
intricate
molecular
mechanisms
underlying
stress
responses,
encompassing
oxidative
stress,
protein
misfolding,
metabolic
reprogramming,
capacity
elicit
adaptive
responses
or
culminate
in
pathological
conditions.
interplay
between
these
organelle
dysfunction
has
implicated
myriad
diseases,
neurodegenerative
disorders,
cancer,
immune-related
pathologies.
A
comprehensive
understanding
by
which
respond
can
offer
valuable
insights
into
therapeutic
strategies
aimed
at
mitigating
damage.
Biomolecules,
Journal Year:
2024,
Volume and Issue:
14(8), P. 919 - 919
Published: July 28, 2024
The
endoplasmic
reticulum
(ER)
is
indispensable
for
maintaining
normal
life
activities.
Dysregulation
of
the
ER
function
results
in
accumulation
harmful
proteins
and
lipids
disruption
intracellular
signaling
pathways,
leading
to
cellular
dysfunction
eventual
death.
Protein
misfolding
within
disrupts
its
delicate
balance,
resulting
misfolded
or
unfolded
proteins,
a
condition
known
as
stress
(ERS).
Renal
fibrosis,
characterized
by
aberrant
proliferation
fibrotic
tissue
renal
interstitium,
stands
grave
consequence
numerous
kidney
disorders,
precipitating
gradual
decline
function.
fibrosis
serious
complication
many
conditions
overgrowth
glomerular
tubular
progressive
failure
Studies
have
shown
that,
during
onset
progression
disease,
ERS
causes
various
problems
kidneys,
process
that
can
lead
fibrosis.
This
article
elucidates
underlying
pathways
modulated
ERS,
delineating
role
triggering
diverse
forms
cell
Additionally,
it
comprehensively
explores
spectrum
potential
pharmacological
agents
molecular
interventions
aimed
at
mitigating
thereby
charting
novel
research
avenues
therapeutic
advancements
management
