International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(12), С. 6778 - 6778
Опубликована: Июнь 20, 2024
Psoriasis
is
a
chronic
inflammatory
condition
affecting
2%
of
the
Western
population.
It
includes
diverse
manifestations
influenced
by
genetic
predisposition,
environmental
factors,
and
immune
status.
The
sustained
activation
mTOR
key
element
in
psoriasis
pathogenesis,
leading
to
an
uncontrolled
proliferation
cytokines.
Furthermore,
has
been
linked
with
transition
from
non-skin
such
as
psoriatic
arthritis
cardiovascular
events.
While
therapies
targeting
pro-inflammatory
cytokines
have
shown
efficacy,
additional
pathways
may
offer
therapeutic
potential.
PI3K/Akt/mTOR
pathway,
known
for
its
role
cell
growth,
proliferation,
metabolism,
emerged
potential
target
psoriasis.
This
review
explores
relevance
pathophysiology,
focusing
on
involvement
cutaneous
atheromatous
plaque
arthritis,
disease.
promotes
keratinocyte
synovial
contributing
formation
joint
inflammation.
Moreover,
exacerbate
risk
promoting
cytokine
production
dysregulation
lipid
glucose
metabolism.
inhibition
promise
preclinical
studies,
reducing
skin
inflammation
proliferation.
mitigate
modulating
cholesterol
metabolism
attenuating
atherosclerosis
progression.
Understanding
psoriasis,
disease
provides
insight
into
treatment
avenues
sheds
light
complex
interplay
metabolic
these
conditions.
The Journal of Immunology,
Год журнала:
2023,
Номер
212(2), С. 302 - 316
Опубликована: Ноя. 29, 2023
Abstract
Immune
cell–derived
IL-17A
is
one
of
the
key
pathogenic
cytokines
in
psoriasis,
an
immunometabolic
disorder.
Although
established
regulator
cutaneous
immune
cell
biology,
its
functional
and
metabolic
effects
on
nonimmune
cells
skin,
particularly
keratinocytes,
have
not
been
comprehensively
explored.
Using
multiomics
profiling
systems
biology–based
approaches,
we
systematically
uncover
significant
roles
for
reprogramming
human
primary
keratinocytes
(HPKs).
High-throughput
liquid
chromatography–tandem
mass
spectrometry
nuclear
magnetic
resonance
spectroscopy
revealed
IL-17A–dependent
regulation
multiple
HPK
proteins
metabolites
carbohydrate
lipid
metabolism.
Systems-level
MitoCore
modeling
using
flux-balance
analysis
identified
IL-17A–mediated
increases
glycolysis,
glutaminolysis,
uptake,
which
were
validated
biochemical
cell-based
assays
stable
isotope-resolved
metabolomics.
treatment
triggered
downstream
mitochondrial
reactive
oxygen
species
HIF1α
expression
resultant
proliferation,
consistent
with
observed
elevation
these
effectors
epidermis
patients
psoriasis.
Pharmacological
inhibition
or
reversed
hyperproliferation.
These
results
identify
as
important
target
reveal
involvement
pathways
skin.
Dermatology Practical & Conceptual,
Год журнала:
2024,
Номер
14(4), С. e2024266 - e2024266
Опубликована: Окт. 30, 2024
Introduction:
In
recent
years,
the
role
of
mammalian
target
rapamycin
(mTOR)
pathway,
which
is
one
intracellular
signaling
pathways
and
known
as
main
control
pathway
metabolism,
in
pathogenesis
psoriasis
has
been
emphasized.
Objectives:
We
sought
to
investigate
importance
mTOR
psoriasis.
Methods:
Forty
patients
with
40
healthy
volunteers
were
included
this
case-control
study.
Serum
fasting
mTORC1
mTORC2
levels
study
groups
examined
by
enzyme-linked
immunosorbent
assay.
Results:
significantly
lower
than
controls
(p=
0.001).
A
positive
correlation
was
found
between
serum
(p=0,001,
r=0,826).
Conclusion:
The
complexes
are
active
signalling
molecules
cell,
be
patient
psoriasis,
suggesting
that
it
may
an
indicator
increased
activation
these
molecules.
Our
opinion
agents
can
effectively
inhibit
both
more
effective
treatment
Frontiers in Immunology,
Год журнала:
2024,
Номер
15
Опубликована: Ноя. 4, 2024
Autophagy
is
a
highly
conserved
cellular
self-digestive
process
that
underlies
the
maintenance
of
homeostasis.
classified
into
three
types:
macrophage,
chaperone-mediated
autophagy
(CMA)
and
microphagy,
which
maintain
homeostasis
through
different
mechanisms.
Altered
regulation
affects
progression
various
skin
diseases,
including
psoriasis
(PA),
systemic
lupus
erythematosus
(SLE),
vitiligo,
atopic
dermatitis
(AD),
alopecia
areata
(AA)
sclerosis
(SSc).
In
this
review,
we
review
existing
literature
focusing
on
mechanisms
autophagy,
namely
as
well
roles
in
above
six
dermatological
disorders
order
to
aid
further
studies
future.
Systemic
lupus
erythematosus
(SLE)
is
a
chronic
autoimmune
disorder
characterized
by
widespread
inflammation
and
multi-organ
damage.
Toll-like
receptor
7
(TLR-7)
autophagy
have
been
implicated
in
SLE
pathogenesis.
Rice
husk
silica
liquid
(RHSL)
has
shown
potential
for
modulating
inflammatory
responses,
but
its
effects
on
not
thoroughly
investigated.
This
study
aims
to
evaluate
the
impact
of
RHSL
immune
responses
an
vitro
model
SLE,
focusing
TLR-7
signaling,
cytokine
production,
modulation.
RAW264.7
cells
human
peripheral
blood
mononuclear
(PBMCs)
from
healthy
donors
patients
were
used.
Cells
stimulated
with
LPS
or
agonists
treated
RHSL.
Cell
viability
was
assessed,
levels
(TNF-α
IL-6)
measured
ELISA.
Autophagy-related
proteins
(LC3II,
ATG5-ATG12)
analyzed
Western
blotting.
The
effect
inhibition
studied
using
3-methyladenine
(3-MA).
did
affect
cell
significantly
reduced
TNF-α
production
LPS-
agonist-stimulated
PBMCs.
enhanced
autophagy,
as
evidenced
increased
LC3II
ATG5-ATG12
conjugation
both
patient-derived
reduction
attenuated
3-MA,
indicating
that
plays
role
this
process.
also
inhibited
translocation
phosphorylated
NF-κB
into
nucleus,
suggesting
mechanism
anti-inflammatory
effects.
exhibits
immunomodulatory
agent
enhancing
signaling
pathways.
These
findings
suggest
could
offer
therapeutic
benefits
managing
warrant
further
investigation
clinical
applications.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(18), С. 10133 - 10133
Опубликована: Сен. 21, 2024
Systemic
lupus
erythematosus
(SLE)
is
a
chronic
autoimmune
disorder
characterized
by
widespread
inflammation
and
multi-organ
damage.
Toll-like
receptor
7
(TLR-7)
autophagy
have
been
implicated
in
SLE
pathogenesis.
Rice
husk
silica
liquid
(RHSL)
has
shown
potential
for
modulating
inflammatory
responses,
but
its
effects
on
not
thoroughly
investigated.
This
study
aims
to
evaluate
the
impact
of
RHSL
immune
responses
cell
culture
experiments,
focusing
TLR-7
signaling,
cytokine
production,
modulation.
RAW264.7
cells
human
peripheral
blood
mononuclear
(PBMCs)
from
healthy
donors
patients
were
used.
Cells
stimulated
with
LPS
or
agonists
treated
RHSL.
Cell
viability
was
assessed,
levels
(TNF-α
IL-6)
measured
ELISA.
Autophagy-related
proteins
(LC3II,
ATG5-ATG12)
analyzed
Western
blotting.
The
effect
inhibition
studied
using
3-methyladenine
(3-MA).
A
concentration
100
μg/mL
did
affect
significantly
reduced
TNF-α
production
agonist-stimulated
(compared
alone,
3.41
±
0.54
vs.
6.72
0.07
folds)
PBMCs
0.97
0.19
1.40
0.33
folds).
enhanced
autophagy,
as
evidenced
increased
LC3II
(4.35
1.08
ATG5-ATG12
(7.07
1.30
conjugation
both
patient-derived
PBMCs.
reduction
attenuated
3-MA,
indicating
that
plays
role
this
process.
also
inhibited
translocation
phosphorylated
NF-κB
into
nucleus,
suggesting
mechanism
anti-inflammatory
effects.
exhibits
an
immunomodulatory
agent
enhancing
signaling
pathways.
These
findings
suggest
could
offer
therapeutic
benefits
managing
warrant
further
investigation
clinical
applications.
