Cells,
Journal Year:
2025,
Volume and Issue:
14(8), P. 565 - 565
Published: April 9, 2025
Background:
Vitiligo
is
featured
by
the
manifestation
of
white
maculae
and
primarily
results
from
inflammatory/immune-selective
aggression
to
melanocytes.
The
trigger
mechanism
leading
activation
resident
immune
cells
in
skin
still
lacks
a
molecular
description.
There
growing
evidence
linking
altered
mitochondrial
metabolism
vitiligo,
suggesting
that
an
underlying
metabolic
defect
may
enable
direct
system.
Recent
demonstrated
association
vitiligo
with
disorders
related
systemic
metabolism,
including
insulin
resistance
(IR)
lipid
disarrangements.
However,
IR,
defined
as
cellular
insulin-mediated
control
glucose
its
possible
role
pathogenesis
has
not
been
proven
yet.
Methods:
In
this
study,
we
compared
Ins/IGF-1
intracellular
signaling
dermal
epidermal
isolated
non-lesional
belonging
obtained
healthy
donors.
Results:
We
due
intensified
uptake,
S6,
receptor
substrate
1
(IRS1)
chronic
phosphorylation,
their
inducibilities
were
downsized,
condition
coincides
definition
at
level.
Correspondingly,
mitogenic
activities
normally
provoked
exposure
resulted
significantly
compromised
(p
≤
0.05).
Besides
all
vitiligo-derived
manifesting
energetic
disequilibrium
consisting
low
ATP,
catabolic
processes
activation,
oxidative
stress,
functional
consequences
state
appear
amplified
keratinocyte
lineage.
Conclusion:
presented
data
argue
for
IGF-1
collocating
dysfunctional
mechanisms
pathogenesis.
keratinocytes,
intrinsic
impairment
activities,
particularly
when
associated
stimulation
Ins/IGF-1,
converges
into
aberrant
pro-inflammatory
phenotype
initiate
cell
recruitment.
Frontiers in Bioscience-Landmark,
Journal Year:
2025,
Volume and Issue:
30(3)
Published: March 18, 2025
Immune
cells
such
as
macrophages
play
a
significant
role
in
ocular
inflammation
by
activating
or
inhibiting
several
cellular
pathways.
Systemic
infections
and
autoimmune
diseases
could
activate
releasing
various
pro-inflammatory
cytokines,
chemokines,
growth
factors,
which
reach
the
eyes
through
blood-retina
barrier
cause
immune
inflammatory
responses.
In
addition,
environmental
pollutants,
allergens,
eye
injuries
also
an
response.
Further,
response
generated
recruit
additional
enhance
The
leads
to
tissue
damage
dysfunction
affects
vision.
Macrophages
are
generally
implicated
clearance
of
pathogens
debris,
generate
reactive
oxygen
species,
initiate
However,
uncontrolled
responses
tissues,
leading
complications
uveitis,
scleritis,
diabetic
retinopathy,
retinitis.
Recent
studies
describe
individual
cytokines
mediation
specific
diseases.
this
article,
we
discussed
potential
impact
their
mediated
on
development
possible
treatment
strategies.
Atherosclerosis Plus,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 1, 2025
Carbonic
anhydrase
I
(CA1)
has
been
reported
to
be
a
diagnostic
and
therapeutic
target
for
atherosclerosis
(AS).
This
study
aimed
verify
the
essential
role
of
CA1
in
AS
progression
CA1-overexpressing
mice.
A
ApoE
[-/-]
knock-in
mouse
model
was
constructed
via
CRISPR/Cas9-mediated
genome
engineering.
then
induced
these
transgenic
mice
administration
high-fat
diet,
second
group
simultaneously
received
treatment
with
methazolamide
(MTZ),
carbonic
inhibitor.
Compared
without
overexpression,
had
greater
average
body
weight,
regardless
whether
their
MTZ
or
induction
status.
Sudan
IV,
hematoxylin
eosin
Oil
Red
O
staining
revealed
more
plaques
fat
deposits
cardiac
aortas
than
those
ordinary
ApoE-/-
when
induced.
Moreover,
atherogenic
index;
low-density
lipoprotein,
total
cholesterol
triglyceride
levels
were
significantly
elevated,
high-density
lipoprotein
declined
peripheral
blood
that
mice,
animals
AS.
Immunohistochemistry,
Von
Kossa
fluorescence
immunohistochemistry
increases
expression,
calcium
deposition
M1
macrophages
aortic
tissues
suppressed
pathologies
above
experiments.
These
findings
aggravated
suggest
aggravates
by
increasing
M1-type
macrophages,
proinflammatory
macrophage
subtype.
Cells,
Journal Year:
2025,
Volume and Issue:
14(8), P. 565 - 565
Published: April 9, 2025
Background:
Vitiligo
is
featured
by
the
manifestation
of
white
maculae
and
primarily
results
from
inflammatory/immune-selective
aggression
to
melanocytes.
The
trigger
mechanism
leading
activation
resident
immune
cells
in
skin
still
lacks
a
molecular
description.
There
growing
evidence
linking
altered
mitochondrial
metabolism
vitiligo,
suggesting
that
an
underlying
metabolic
defect
may
enable
direct
system.
Recent
demonstrated
association
vitiligo
with
disorders
related
systemic
metabolism,
including
insulin
resistance
(IR)
lipid
disarrangements.
However,
IR,
defined
as
cellular
insulin-mediated
control
glucose
its
possible
role
pathogenesis
has
not
been
proven
yet.
Methods:
In
this
study,
we
compared
Ins/IGF-1
intracellular
signaling
dermal
epidermal
isolated
non-lesional
belonging
obtained
healthy
donors.
Results:
We
due
intensified
uptake,
S6,
receptor
substrate
1
(IRS1)
chronic
phosphorylation,
their
inducibilities
were
downsized,
condition
coincides
definition
at
level.
Correspondingly,
mitogenic
activities
normally
provoked
exposure
resulted
significantly
compromised
(p
≤
0.05).
Besides
all
vitiligo-derived
manifesting
energetic
disequilibrium
consisting
low
ATP,
catabolic
processes
activation,
oxidative
stress,
functional
consequences
state
appear
amplified
keratinocyte
lineage.
Conclusion:
presented
data
argue
for
IGF-1
collocating
dysfunctional
mechanisms
pathogenesis.
keratinocytes,
intrinsic
impairment
activities,
particularly
when
associated
stimulation
Ins/IGF-1,
converges
into
aberrant
pro-inflammatory
phenotype
initiate
cell
recruitment.
