Targeting PIM1 by Bruceine D attenuates skin fibrosis via myofibroblast ferroptosis
Jianzhang Wang,
Yajuan Song,
Xiao-Ying Tan
и другие.
Redox Biology,
Год журнала:
2025,
Номер
unknown, С. 103619 - 103619
Опубликована: Март 1, 2025
Язык: Английский
Double-edged sword effect of GPX4 in skin homeostasis and diseases
Archives of Dermatological Research,
Год журнала:
2025,
Номер
317(1)
Опубликована: Фев. 14, 2025
Язык: Английский
Increased melanin induces aberrant keratinocyte − melanocyte − basal − fibroblast cell communication and fibrogenesis by inducing iron overload and ferroptosis resistance in keloids
Cell Communication and Signaling,
Год журнала:
2025,
Номер
23(1)
Опубликована: Март 18, 2025
Keloid
is
a
typical
skin
fibrotic
disease
with
unclear
mechanisms
and
limited
therapeutic
options.
Fibroblast-induced
fibrogenesis
crucial
cause
of
KD.
However,
the
types
cells
involved
in
fibroblast
KD
specific
are
unclear.
This
study
aimed
to
investigate
role
melanocyte-secreted
melanin
promoting
its
mechanism
evaluate
potential
effect
intervening
treating
keloid.
The
activity
pigmentation-related
pathways
melanocytes
was
examined
using
single-cell
RNA-sequence
(scRNA-seq)
analysis.
Masson-Fontana
staining
or
isolated
quantification
detected
levels
distribution
cells.
Collagen
deposition,
wounding
healing,
proliferation
analysis
were
employed
integratively
assess
fibrogenesis.
After
treatment,
bulk-seq
identified
fibroblasts'
differentially
expressed
genes
(DEGs).
iron
by
Perl's
quantification.
Cell
viability,
LipidROS,
malondialdehyde
assay
accessed
ferroptosis
levels.
ML329
evaluated
keloid-bearing
mice.
We
found
enriched
keloid
further
validated
increased
patients.
Additionally,
positively
correlated
Area
Severity
Index
Furthermore,
significantly
promoted
proliferation,
migration,
collagen
synthesis.
Mechanically,
basal
cell
permeability
inflammation
facilitate
transfer
dermis,
where
it
activated
fibroblasts
evoking
overload
resistance.
Consistently,
resistance
primary
tissues
Inhibition
effectively
diminish
melanin-induced
Interestingly,
induced
an
autocrine
manner
stimulated
keratinocytes
take
up
deepen
color
upregulating
F2R-like
trypsin
receptor
1
(F2RL1).
In
vivo,
delivery
ML329,
microphthalmia-associated
transcription
factor
(MITF)
inhibitor,
could
suppress
melanogenesis
alleviate
human
nude
Meanwhile,
decreased
content
restored
sensitivities
ferroptosis.
Collectively,
melanin-lowing
strategies
may
appear
as
new
target
for
Current
treatments
ineffective.
Our
research
demonstrates
that
increase
patients
play
significant
progression
mediating
aberrant
keratinocyte
−
melanocyte
crosstalk.
Importantly,
we
pharmacological
inhibition
MITF
shows
promise
alleviating
keloid,
offering
breakthrough
treatment.
synthesis
pathway
abnormally
melanocytes.
Melanin
destroys
membrane
barrier
triggering
translocates
dermal
layers
paracrine
induce
overgrowth,
ECM
deposition
inducing
maintains
melanocytes'
hyperproliferative
non-immortal
properties
manner.
It
enhances
keratocyte
PAR-2
promote
transit
superficial
epidermis
layers,
which
be
related
deepening
color.
alleviates
Язык: Английский
Skin Aging and the Upcoming Role of Ferroptosis in Geroscience
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(15), С. 8238 - 8238
Опубликована: Июль 28, 2024
The
skin
is
considered
the
most
important
organ
system
in
mammals,
and
as
population
ages,
it
to
consider
aging
anti-aging
therapeutic
strategies.
Exposure
of
various
insults
induces
significant
changes
throughout
our
lives,
differentiating
a
young
adult
from
that
an
older
adult.
These
are
caused
by
combination
intrinsic
extrinsic
aging.
We
report
interactions
between
its
metabolism,
showing
network
due
several
factors.
For
example,
iron
nutrient
for
humans,
but
level
increases
with
aging,
inducing
deleterious
effects
on
cellular
functions.
Recently,
was
discovered
ferroptosis,
or
iron-dependent
cell
death,
linked
diseases.
pursuit
new
molecular
targets
ferroptosis
has
recently
attracted
attention.
Prevention
effective
strategy
treatment
diseases,
especially
old
age.
However,
pathological
biological
mechanisms
underlying
still
not
fully
understood,
diseases
such
melanoma
autoimmune
Only
few
basic
studies
regulated
death
exist,
challenge
turn
into
clinical
applications.
Язык: Английский
Increased melanin induces aberrant keratinocyte−melanocyte−basal−fibroblast cell communication and fibrogenesis by inducing iron overload and ferroptosis resistance in keloids
Research Square (Research Square),
Год журнала:
2024,
Номер
unknown
Опубликована: Ноя. 15, 2024
Abstract
Keloid
is
a
typical
skin
fibrotic
disease
with
unclear
mechanisms
and
limited
therapeutic
options.
In
this
study,
we
found
the
enriched
pigmentation-related
pathways
in
melanocytes
of
keloid
by
single-cell
RNA-sequence
(scRNA-seq)
analysis.
We
further
validated
increased
melanin
levels
patients.
Additionally,
positively
correlated
Area
Severity
Index
keloid.
Furthermore,
melanocyte-secreted
significantly
promoted
fibroblast
proliferation,
migration,
collagen
synthesis.
Mechanically,
basal
cell
permeability
inflammation
to
facilitate
its
transfer
dermis,
where
it
activated
fibroblasts
evoking
iron
overload
ferroptosis
resistance.
Consistently,
resistance
were
primary
tissues
Inhibition
effectively
diminish
melanin-induced
fibrogenesis.
Interestingly,
induced
an
autocrine
manner
stimulated
keratinocytes
take
up
deepen
color
upregulating
F2R-like
trypsin
receptor
1
(F2RL1).
In
vivo,
delivery
ML329,
micropthalmia-associated
transcription
factor
(MITF)
inhibitor,
could
suppress
melanogenesis
alleviate
human
keloid-bearing
nude
mice.
Meanwhile,
ML329
decreased
content
restored
sensitivities
ferroptosis.
Collectively,
melanin-lowing
strategies
may
appear
as
potential
new
target
for
Язык: Английский
Viral Infections and the Glutathione Peroxidase Family: Mechanisms of Disease Development
Antioxidants and Redox Signaling,
Год журнала:
2024,
Номер
unknown
Опубликована: Окт. 24, 2024
The
glutathione
peroxidase
(GPx)
family
is
recognized
for
its
essential
function
in
maintaining
cellular
redox
balance
and
countering
the
overproduction
of
reactive
oxygen
species
(ROS),
a
process
intricately
linked
to
progression
various
diseases
including
those
spurred
by
viral
infections.
modulation
GPx
activity
viruses
presents
critical
juncture
disease
pathogenesis,
influencing
responses
trajectory
infection-induced
diseases.
Язык: Английский