AbstractSilicosis
is
one
of
the
most
common
and
rapidly
progressing
occupational
diseases
in
world,
there
still
no
specific
drug
to
reverse
end-stage
diffuse
interstitial
fibrosis.
Strikingly,
crosstalk
between
macrophages
fibroblasts
plays
a
vital
role
development
silicosis
Here
we
study
nano-miniaturization
natural
compounds,
proanthocyanidins,
alleviate
via
mediating
interaction
above
cells.
In
this
study,
proanthocyanidins
were
loaded
into
mesoporous
Prussian
blue
coated
by
hyaluronic
acid-inserted
macrophage
membrane,
termed
as
HMP@PC
NPs.
vitro,
macrophages-targeted
NPs
inhibits
activation
blunting
M1/M2
polarization
accordingly
inflammatory
cytokines
co-culture
system.
vivo,
safety
not
only
alleviates
SiO2-induced
fibrosis,
but
also
remodel
benign
intestinal
microbiota
homeostasis
corresponding
non-targeted
metabolites.
These
findings
could
benefit
for
potential
therapeutic
strategy
treat
MedComm,
Journal Year:
2025,
Volume and Issue:
6(3)
Published: Feb. 23, 2025
Ferroptosis
is
a
distinct
form
of
iron-dependent
programmed
cell
death
characterized
primarily
by
intracellular
iron
accumulation
and
lipid
peroxidation.
Multiple
cellular
processes,
including
amino
acid
metabolism,
various
signaling
pathways,
autophagy,
have
been
demonstrated
to
influence
the
induction
progression
ferroptosis.
Recent
investigations
elucidated
that
ferroptosis
plays
crucial
role
in
pathogenesis
pulmonary
disorders,
lung
injury,
chronic
obstructive
disease,
fibrosis,
asthma.
increasingly
recognized
as
promising
novel
strategy
for
cancer
treatment.
Various
immune
cells
within
tumor
microenvironment,
CD8+
T
cells,
macrophages,
regulatory
natural
killer
dendritic
shown
induce
modulate
process
through
regulation
metabolism
pathways.
Conversely,
can
reciprocally
alter
metabolic
environment,
leading
activation
or
inhibition
functions,
thereby
modulating
responses.
This
paper
reviews
molecular
mechanism
describes
discusses
connection
between
microenvironment
diseases,
development
prospect
their
interaction
treatment
diseases.
Pharmaceuticals,
Journal Year:
2025,
Volume and Issue:
18(3), P. 334 - 334
Published: Feb. 26, 2025
In
recent
years,
ferroptosis,
as
an
emerging
modality
of
programmed
cell
death,
has
captured
significant
attention
within
the
scientific
community.
This
comprehensive
review
meticulously
canvasses
pertinent
literature
past
few
spanning
multiple
facets.
It
delves
into
intricate
mechanisms
underpinning
tracks
evolution
its
inducers
and
inhibitors,
dissects
roles
in
a
diverse
array
diseases,
well
resultant
therapeutic
implications.
A
profound
exploration
is
conducted
functional
ferroptosis-related
molecules,
intracellular
pathways,
metabolic
cascades,
signaling
transduction
routes.
Novel
ferroptosis
inhibitors
are
introduced
detail,
covering
their
design
blueprints,
synthetic
methodologies,
bioactivity
profiles.
Moreover,
exhaustive
account
provided
regarding
involvement
malignancies,
neurodegenerative
disorders,
cardiovascular
ailments,
other
pathologies.
By
highlighting
pivotal
status
potential
regimens
various
this
aspires
to
furnish
thorough
reference
framework
for
future
investigations
clinical
translations
domain.
Advanced Healthcare Materials,
Journal Year:
2024,
Volume and Issue:
13(28)
Published: July 16, 2024
Abstract
Increased
inflammatory
responses
and
oxidative
stress
at
the
wound
site
following
skin
trauma
impair
healing.
Furthermore,
scarring
places
fibroblasts
under
severe
mechanical
aggravates
pathological
fibrosis.
A
novel
liposomal
composite
hydrogel
is
engineered
for
microenvironment
remodeling,
incorporating
dual‐loaded
liposomes
into
gelatin
methacrylate
to
create
a
nanocomposite
hydrogel.
Notably,
tetrahydrocurcumin
(THC)
hepatocyte
growth
factor
(HGF)
are
encapsulated
in
hydrophobic
hydrophilic
layers
of
liposomes,
respectively.
The
maintains
porous
nanoarchitecture,
demonstrating
sustainable
THC
HGF
release
enhanced
properties
biocompatibility.
This
system
effectively
promotes
cell
proliferation
angiogenesis
attenuates
apoptosis.
It
decreases
expression
factors
by
inhibiting
high‐mobility
group
box
/receptor
advanced
glycation
end
product/NF‐κB
(HMGB1/RAGE/NF‐κB)pathway
increases
macrophage
polarization
from
M1
M2
vitro,
controlling
responses.
exhibits
remarkable
antioxidant
scavenging
excess
reactive
oxygen
species
free
radicals.
Most
importantly,
it
prevents
scar
formation
restraining
transforming
beta
(TGF‐β)/Smads
pathway
that
downregulates
associated
fibrotic
factors.
demonstrates
strong
therapeutic
effects
against
inflammation
fibrosis
rat
model
with
biosafety,
advancing
development
innovative
hydrogel‐based
delivery
strategies
clinical
scarless
therapy.
MedComm,
Journal Year:
2024,
Volume and Issue:
5(10)
Published: Sept. 23, 2024
Abstract
Pulmonary
fibrosis
(PF)
is
a
chronic
and
progressive
lung
disease
characterized
by
extensive
alterations
of
cellular
fate
function
excessive
accumulation
extracellular
matrix,
leading
to
tissue
scarring
impaired
respiratory
function.
Although
our
understanding
its
pathogenesis
has
increased,
effective
treatments
remain
scarce,
fibrotic
progression
major
cause
mortality.
Recent
research
identified
various
etiological
factors,
including
genetic
predispositions,
environmental
exposures,
lifestyle
which
contribute
the
onset
PF.
Nonetheless,
precise
mechanisms
these
factors
interact
drive
are
not
yet
fully
elucidated.
This
review
thoroughly
examines
diverse
molecular
mechanisms,
key
signaling
pathways
involved
in
PF,
such
as
TGF‐β,
WNT/β‐catenin,
PI3K/Akt/mTOR.
It
also
discusses
current
therapeutic
strategies,
antifibrotic
agents
like
pirfenidone
nintedanib,
explores
emerging
targeting
senescence.
Emphasizing
need
for
omni‐target
approaches
overcome
limitations
therapies,
this
integrates
recent
findings
enhance
PF
development
more
prevention
management
ultimately
improving
patient
outcomes.
Frontiers in Medicine,
Journal Year:
2025,
Volume and Issue:
12
Published: Feb. 24, 2025
Respiratory
diseases
rank
among
the
foremost
causes
of
mortality
and
disability
globally,
with
long-term
exposure
to
environmental
pollutants
playing
a
critical
role
in
their
onset
progression.
Despite
this,
underlying
mechanisms
effective
targeted
treatments
for
these
disorders
remain
poorly
understood,
highlighting
an
urgent
need
focused
research.
Cell
death,
programmed
cellular
response
external
harmful
stimuli,
including
ferroptosis-a
recently
identified
form
iron-dependent
cell
death-emerges
as
pivotal
process.
Characterized
by
intracellular
iron
accumulation
lipid
peroxidation,
ferroptosis
appears
intricately
linked
lung
injury
induced
pollutants.
This
review
examines
triggered
factors,
aiming
shed
light
on
its
specific
pathophysiological
potential
therapeutic
target.
By
deepening
our
understanding
interactions
between
pollution,
ferroptosis,
damage,
we
hope
inform
strategies
intervention.