Journal of Inflammation Research,
Год журнала:
2024,
Номер
Volume 17, С. 10495 - 10513
Опубликована: Дек. 1, 2024
Background:
Peripheral
biomarkers
are
becoming
an
important
method
by
which
to
monitor
the
progression
of
coronary
artery
disease
(CAD).
Not
only
they
minimally
invasive
and
early
detection,
but
can
also
be
used
for
classification
diagnosis
as
well
prognostic
assessment.
Currently,
this
approach
is
still
in
exploratory
stage.
The
purpose
research
determine
diagnostic
value
therapeutic
potential
endoplasmic
reticulum
stress
(ERS)
genes
CAD.
Methods:
clinical
information
RNA
sequence
data
were
obtained
from
GEO
database
subsequently
subjected
a
series
optimization
visualization
processes
using
various
analytical
techniques,
including
WGCNA,
LASSO,
SVM-RFE
feature
selection,
random
forest
(RF),
XGBoost,
R
software
Cytoscape.
Finally,
immunofluorescence
was
validate
analysis.
Results:
We
identify
6
key
ERS
differentially
expressed
(ERS-DEGs)
(UFL1,
HSPA1A,
ERLIN1,
LRRK2,
ERN1,
SERINC3)
constructing
models.
They
showed
qualified
ability
CAD
within
training
dataset
(AUC
=
0.803)
validation
0.776
0.797).
Association
analyses
that
peripheral
immune
cells,
checkpoint
Human
Leukocyte
Antigen
(HLA)
had
characteristic
distributions
closely
related
specific
genes.
Meanwhile,
we
found
HSPA1A
may
involve
MAPK
signaling
pathway
Conclusion:
constructed
efficient
model
based
on
ERS-DEGs
explored
their
regulatory
networks
effects
microenvironment.
UFL1,
SERINC3
expected
Keywords:
stress,
disease,
microenvironment
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(8), С. 4368 - 4368
Опубликована: Апрель 15, 2024
Dynamic
regulation
of
the
cellular
proteome
is
mainly
controlled
in
endoplasmic
reticulum
(ER).
Accumulation
misfolded
proteins
due
to
ER
stress
leads
activation
unfolded
protein
response
(UPR).
The
primary
role
UPR
reduce
bulk
damages
and
try
drive
back
system
former
or
a
new
homeostatic
state
by
autophagy,
while
an
excessive
level
results
apoptosis.
It
has
already
been
proven
that
proper
order
characteristic
features
both
surviving
self-killing
mechanisms
are
negative
positive
feedback
loops,
respectively.
suggest
these
loops
found
not
only
within
but
also
between
branches
UPR,
fine-tuning
stress.
In
this
review,
we
summarize
recent
knowledge
dynamical
mechanism
using
theoretical
molecular
biological
techniques.
addition,
review
pays
special
attention
describing
action
controlling
life-and-death
decision
upon
Since
appears
diseases
common
worldwide,
more
detailed
understanding
behaviour
medical
importance.
Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids,
Год журнала:
2024,
Номер
1869(7), С. 159515 - 159515
Опубликована: Июнь 5, 2024
Although
our
current
knowledge
of
the
molecular
crosstalk
between
ER
stress,
unfolded
protein
response
(UPR),
and
lipid
homeostasis
remains
limited,
there
is
increasing
evidence
that
dysregulation
either
or
profoundly
affects
other.
Most
research
regarding
UPR
signaling
in
human
diseases
has
focused
on
causes
consequences
disrupted
folding.
The
itself
consists
very
complex
pathways
function
to
not
only
maintain
homeostasis,
but
just
as
importantly,
modulate
biogenesis
allow
adjust
promote
cell
survival.
Lipid
known
activate
many
aspects
UPR,
complexity
this
a
major
barrier.
disequilibrium
lipotoxicity
are
be
important
contributors
numerous
pathologies,
including
insulin
resistance,
liver
disease,
cardiovascular
diseases,
neurodegenerative
cancer.
Despite
their
medical
significance
continuous
research,
however,
mechanisms
synthesis
during
stress
conditions,
impact
fate
decisions,
remain
poorly
understood.
Here
we
summarize
view
connections
altered
metabolism,
UPR.
Cell Stress and Chaperones,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 1, 2025
Acute
pancreatitis
(AP)
is
associated
with
multiple
cellular
mechanisms
that
trigger
and
or
are
triggered
by
the
inflammatory
injury
death
of
acinar
cells.
One
key
endoplasmic
reticulum
(ER)
stress
which
manifests
as
an
accumulation
misfolded
proteins
within
ER,
event
has
pro-inflammatory
proapoptotic
consequences.
Hence,
degree
cell
insult
during
AP
could
considerably
depend
on
signaling
pathways
upregulated
ER
its
resulting
dyshomeostasis
such
C/EBP
homologous
protein
(CHOP),
cJUN
NH2-terminal
kinase
(JNK),
nuclear
factor
kappa
B
(NF-κB),
NOD-like
receptor
3
(NLRP3)
inflammasome.
Exploring
these
molecular
interesting
area
for
translational
medicine
it
may
lead
to
identifying
new
therapeutic
targets
in
AP.
This
review
literature
aims
shed
light
different
roles
etiopathogenesis
pathogenesis
Then,
specifically
focuses
implications
this
context.
International Journal of Molecular Sciences,
Год журнала:
2025,
Номер
26(7), С. 3398 - 3398
Опубликована: Апрель 5, 2025
Heart
failure
and
diabetes
mellitus
are
major
contributors
to
global
morbidity
mortality,
with
their
prevalence
continuously
rising,
primarily
due
aging
populations
improvements
in
healthcare.
These
conditions
often
coexist
or
develop
sequentially,
leading
complex
interactions
that
significantly
influence
the
progression
management
of
both
diseases.
Furthermore,
heart
commonly
associated
coronary
artery
disease,
which
presents
a
unique
challenge
clinical
management,
particularly
context
myocardial
revascularization.
The
presence
exacerbates
atherosclerotic
impairs
endothelial
function,
while
complicates
perfusion
recovery
tissue
post-intervention.
This
narrative
review
delves
into
underlying
mechanisms
contributing
revascularization
patients
diabetes,
emphasizing
importance
understanding
these
for
optimal
treatment.
also
summarizes
key
findings
from
randomized
controlled
trials,
examining
evidence
general
population
specific
subgroups,
including
elderly
left
main
chronic
kidney
peripheral
obstructive
pulmonary
disease.
Understanding
complexities
is
critical
improving
patient
outcomes.
Frontiers in Pharmacology,
Год журнала:
2024,
Номер
15
Опубликована: Июль 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
Translational Cancer Research,
Год журнала:
2024,
Номер
13(7), С. 3760 - 3770
Опубликована: Июль 1, 2024
Background:
Endoplasmic
reticulum
stress
(ERS)-related
genes
are
related
to
tumor
growth,
metastasis,
and
immunotherapy
response.
In
this
paper,
we
tried
identify
ERS-related
in
colon
cancer.
Methods:
were
downloaded
from
the
Molecular
Signatures
Database
(MSigDB)
GeneCards
websites.
Normal
samples
of
obtained
The
Cancer
Genome
Atlas
(TCGA),
Genotype-Tissue
Expression
Project
(GTEx),
Gene
Omnibus
(GEO)
databases.
A
risk
model
based
on
gene
coefficients
was
constructed
by
using
least
absolute
shrinkage
selection
operator
(LASSO)
regression.
inherent
biological
process
differences
between
groups
explored
Ontology
(GO)
set
enrichment
analysis
(GSEA).
ESTIMATE
single-sample
GSEA
(ssGSEA)
algorithms
used
analyze
correlation
microenvironment
(TME)
immune
checkpoint
score.
semi-inhibitory
concentration
(IC50)
values
chemotherapeutic
drugs
calculated
evaluate
sensitivity
immunotherapy.
Results:
pathway
showed
that
ERS
relevant
biosynthesis
metabolism.
Consistent
clustering
differentially
expressed
(DEGs)
demonstrated
divided
into
three
clusters
had
significant
clinicopathological
differences.
consisting
six
established.
verified
GSE39582
GSE17536
testing
datasets.
results
significantly
TME
checkpoint,
these
enhanced
ability
Conclusions:
We
established
a
with
(PMM2,
STC2,
EIF2AK1,
HSPA1A,
SLC8A1,
KCNQ1),
which
enhance
for
These
may
provide
new
perspective
treatment
