Current Pharmaceutical Design,
Год журнала:
2023,
Номер
30(3), С. 180 - 214
Опубликована: Дек. 28, 2023
Introduction:
This
narrative
review
addresses
the
clinical
challenges
in
stress-related
disorders
such
as
depression,
focusing
on
interplay
between
neuron-specific
and
pro-inflammatory
mechanisms
at
cellular,
cerebral,
systemic
levels.
Objective:
We
aim
to
elucidate
molecular
linking
chronic
psychological
stress
with
low-grade
neuroinflammation
key
brain
regions,
particularly
roles
of
G
proteins
serotonin
(5-HT)
receptors.
Methods:
comprehensive
literature
employs
systematic,
narrative,
scoping
methodologies,
combined
approaches
general
pathology.
It
synthesizes
current
research
shared
signaling
pathways
involved
responses
neuroinflammation,
including
calcium-dependent
mechanisms,
mitogen-activated
protein
kinases,
transcription
factors
like
NF-κB
p53.
The
also
focuses
role
protein-coupled
neurotransmitter
receptors
(GPCRs)
immune
responses,
a
detailed
analysis
how
13
14
types
human
5-HT
contribute
depression
neuroinflammation.
Results:
reveals
complex
interaction
signals
immunoinflammatory
pathologies.
highlights
GPCRs
canonical
inflammatory
mediators
influencing
both
pathological
physiological
processes
nervous
tissue.
Conclusion:
proposed
Neuroimmunoinflammatory
Stress
Model
(NIIS
Model)
suggests
that
proinflammatory
pathways,
mediated
by
metabotropic
ionotropic
receptors,
are
crucial
for
maintaining
neuronal
homeostasis.
Chronic
mental
can
disrupt
this
balance,
leading
increased
states
contributing
neuropsychiatric
psychosomatic
disorders,
depression.
model
integrates
traditional
theories
pathogenesis,
offering
understanding
multifaceted
nature
condition.
Biomedicines,
Год журнала:
2022,
Номер
10(11), С. 2703 - 2703
Опубликована: Окт. 26, 2022
Cellular
senescence
is
linked
with
chemotherapy
resistance.
Based
on
previous
studies,
GRP78
a
signal
transducer
in
senescent
cells.
However,
the
association
between
and
stem
cell
phenotype
remains
unknown.
Cisplatin
treatment
was
clarified
to
induce
cellular
leading
stemness
induction
via
GRP78/Akt
transduction.
H460
cells
were
treated
5
μM
of
cisplatin
for
6
days
develop
senescence.
The
colony
formation
assay
cycle
analysis
performed.
SA-β-galactosidase
staining
indicated
Western
blot
RT-PCR
operated.
Immunoprecipitation
(IP)
immunocytochemistry
assays
(ICC)
also
Colony-forming
activity
completely
inhibited,
87.07%
population
arrested
G2
phase
cycle.
mRNA
p21
p53
increased
approximately
by
15.91-
19.32-fold,
respectively.
protein
level
elevated
9.57-
5.9-fold,
In
addition,
c-Myc
decreased
0.2-fold
when
compared
non-treatment
control.
Even
though,
total
downregulated
after
treatment,
but
MTJ1
downstream
regulator,
p-Akt/Akt
ratio
upregulated
3.38
1.44-fold,
found
at
surface
membrane.
Results
showed
that
GRP78/MTJ1
complex
markers,
including
CD44,
CD133,
Nanog,
Oct4,
Sox2,
concomitantly
anchored
GRP78,
facilitating
transduction
stem-like
phenotypes.
strategy
could
interrupt
binding
these
crucial
proteins
or
inhibit
translocation
might
beuseful
cancer
therapy.
Journal of Clinical Immunology,
Год журнала:
2022,
Номер
42(4), С. 783 - 797
Опубликована: Март 8, 2022
Ataxia
telangiectasia
(AT)
is
a
rare
neurodegenerative
genetic
disorder
due
to
bi-allelic
mutations
in
the
Telangiectasia
Mutated
(ATM)
gene.
The
aim
of
this
paper
better
define
immunological
profile
over
time,
clinical
immune-related
manifestations
at
diagnosis
and
during
follow-up,
attempt
genotype-phenotype
correlation
an
Italian
cohort
AT
patients.
Retrospective
data
69
patients
diagnosed
between
December
1984
November
2019
were
collected
from
database
Primary
Immunodeficiency
Network.
Patients
classified
as
lymphopenic
(Group
A)
or
non-lymphopenic
B).
Fifty
eight
out
(84%)
genetically
characterized
distinguished
according
type
truncating/truncating
(TT;
27
patients),
non-truncating
(NT)/T
(28
NT/NT
(5
patients).
In
3
patients,
only
one
mutation
was
detected.
Data
on
age
onset
diagnosis,
cellular
humoral
compartment
infectious
diseases,
signs
immune
dysregulation,
cancer,
survival
analyzed
compared
genotype.
Lymphopenia
related
per
se
earlier
onset.
Progressive
reduction
occurred
follow-up
with
gradual
T
B
cell
number.
Most
Group
A
carried
truncating
mutations,
had
more
severe
lymphopenia,
reduced
life
expectancy.
trend
higher
frequency
interstitial
lung
disease,
malignancy
noted
T/T
genotype
are
associated
worst
course.
Several
mechanisms
may
underlie
premature
progressive
decline
subjects.
Frontiers in Cell and Developmental Biology,
Год журнала:
2021,
Номер
9
Опубликована: Дек. 8, 2021
Angiotensin
II
can
cause
oxidative
stress
and
increased
blood
pressure
that
result
in
long
term
cardiovascular
pathologies.
Here
we
evaluated
the
contribution
of
cellular
senescence
to
effect
chronic
exposure
low
dose
angiotensin
a
model
mimics
tissue
damage.
We
utilized
INK-ATTAC
(p16
Ink4a
–Apoptosis
Through
Targeted
Activation
Caspase
8)
transgenic
mouse
allows
for
conditional
elimination
p16
-dependent
senescent
cells
by
administration
AP20187.
treatment
3
weeks
induced
ATTAC
transgene
expression
kidneys
but
not
lung,
spleen
brain
tissues.
In
ATM,
p15
p21
matched
with
induction
senescence-associated
secretory
phenotype
genes
MMP3,
FGF2,
IGFBP2,
tPA.
Senescent
were
identified
as
endothelial
detection
GFP
expressed
from
angiopoietin
2
von
Willebrand
Factor,
indicative
cell
Furthermore,
inflammation-related
glycoprotein
versican
immune
recruitment
kidneys.
AP20187-mediated
p16-dependent
prevented
physiologic,
molecular
responses
provides
mechanistic
evidence
driver
effects.
Current Pharmaceutical Design,
Год журнала:
2023,
Номер
30(3), С. 180 - 214
Опубликована: Дек. 28, 2023
Introduction:
This
narrative
review
addresses
the
clinical
challenges
in
stress-related
disorders
such
as
depression,
focusing
on
interplay
between
neuron-specific
and
pro-inflammatory
mechanisms
at
cellular,
cerebral,
systemic
levels.
Objective:
We
aim
to
elucidate
molecular
linking
chronic
psychological
stress
with
low-grade
neuroinflammation
key
brain
regions,
particularly
roles
of
G
proteins
serotonin
(5-HT)
receptors.
Methods:
comprehensive
literature
employs
systematic,
narrative,
scoping
methodologies,
combined
approaches
general
pathology.
It
synthesizes
current
research
shared
signaling
pathways
involved
responses
neuroinflammation,
including
calcium-dependent
mechanisms,
mitogen-activated
protein
kinases,
transcription
factors
like
NF-κB
p53.
The
also
focuses
role
protein-coupled
neurotransmitter
receptors
(GPCRs)
immune
responses,
a
detailed
analysis
how
13
14
types
human
5-HT
contribute
depression
neuroinflammation.
Results:
reveals
complex
interaction
signals
immunoinflammatory
pathologies.
highlights
GPCRs
canonical
inflammatory
mediators
influencing
both
pathological
physiological
processes
nervous
tissue.
Conclusion:
proposed
Neuroimmunoinflammatory
Stress
Model
(NIIS
Model)
suggests
that
proinflammatory
pathways,
mediated
by
metabotropic
ionotropic
receptors,
are
crucial
for
maintaining
neuronal
homeostasis.
Chronic
mental
can
disrupt
this
balance,
leading
increased
states
contributing
neuropsychiatric
psychosomatic
disorders,
depression.
model
integrates
traditional
theories
pathogenesis,
offering
understanding
multifaceted
nature
condition.
