International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
26(1), С. 27 - 27
Опубликована: Дек. 24, 2024
The
inflammatory
response
consists
of
two
stages:
priming
and
triggering.
triggering
stage
is
marked
by
the
activation
inflammasomes,
which
are
cytosolic
protein
complexes
acting
as
platforms
for
inflammation.
Inflammasomes
divided
into
canonical
noncanonical
categories.
Inflammatory
lung
diseases
such
asthma,
chronic
obstructive
pulmonary
disease
(COPD),
acute
respiratory
distress
syndrome
(ARDS),
injury,
fibrosis
arise
from
inflammation
damage.
While
role
inflammasomes
in
these
well
demonstrated,
recent
findings
emphasize
critical
roles
regulating
various
conditions.
Particularly,
new
studies
highlight
their
involvement
diseases.
This
review
delves
research
on
regulatory
human
caspase-4
murine
caspase-11,
development
diseases,
potential
targeting
treatments.
JAMA,
Год журнала:
2024,
Номер
332(5), С. 380 - 380
Опубликована: Май 19, 2024
Current
treatments
for
idiopathic
pulmonary
fibrosis
slow
the
rate
of
lung
function
decline,
but
may
be
associated
with
adverse
events
that
affect
medication
adherence.
In
phase
2
trials,
pamrevlumab
(a
fully
human
monoclonal
antibody
binds
to
and
inhibits
connective
tissue
growth
factor
activity)
attenuated
progression
without
substantial
events.
Pharmaceuticals,
Год журнала:
2024,
Номер
17(6), С. 709 - 709
Опубликована: Май 30, 2024
Pirfenidone
and
Nintedanib
are
specific
drugs
used
against
idiopathic
pulmonary
fibrosis
(IPF)
that
showed
efficacy
in
non-IPF
fibrosing
interstitial
lung
diseases
(ILD).
Both
have
side
effects
affect
patients
different
ways
levels
of
severity,
making
treatment
even
more
challenging
for
clinicians.
The
present
review
aims
to
assess
the
effectiveness
potential
complications
regimens
across
various
ILD
diseases.
A
detailed
search
was
performed
relevant
articles
published
between
2018
2023
listed
PubMed,
UpToDate,
Google
Scholar,
ResearchGate,
supplemented
with
manual
research.
following
keywords
were
searched
databases
all
possible
combinations:
Nintedanib;
Pirfenidone,
disease,
fibrosis.
most
widely
accepted
method
evaluating
progression
is
through
decline
forced
vital
capacity
(FVC),
as
determined
by
respiratory
function
tests.
Specifically,
a
decrease
FVC
over
6–12-month
period
correlates
directly
increased
mortality
rates.
Antifibrotic
been
extensively
validated;
however,
some
reported
several
effects,
predominantly
gastrointestinal
symptoms
(such
diarrhea,
dyspepsia,
vomiting),
well
photosensitivity
skin
rashes,
particularly
associated
Pirfenidone.
In
cases
where
extremely
severe
threatening
than
disease
itself,
has
be
discontinued.
However,
further
research
needed
optimize
use
antifibrotic
agents
PF-ILDs,
which
could
slow
all-cause
mortality.
Finally,
other
studies
requested
establish
treatments
can
stop
progression.
Cell Biochemistry and Biophysics,
Год журнала:
2025,
Номер
unknown
Опубликована: Фев. 19, 2025
Abstract
Idiopathic
Pulmonary
Fibrosis
(IPF)
is
a
severe,
rapidly
advancing
disease
that
drastically
diminishes
life
expectancy.
Without
treatment,
it
can
progress
to
lung
cancer.
The
precise
etiology
of
IPF
remains
unknown,
but
inflammation
and
damage
the
alveolar
epithelium
are
widely
thought
be
pivotal
in
its
development.
Research
has
indicated
activating
NLRP3
inflammasome
crucial
mechanism
pathogenesis,
as
triggers
release
pro-inflammatory
cytokines
such
IL-1β,
IL-18,
TGF-β.
These
contribute
myofibroblast
differentiation
extracellular
matrix
(ECM)
accumulation.
Currently,
treatment
options
for
limited.
Only
two
FDA-approved
medications,
pirfenidone
nintedanib,
available.
While
these
drugs
decelerate
progression,
they
come
with
range
side
effects
do
not
cure
disease.
Additional
strategies
primarily
involve
supportive
care
therapy.
Emerging
research
highlighted
numerous
flavonoids
derived
from
traditional
medicines
inhibit
critical
regulators
responsible
inflammasome.
show
promise
potential
therapeutic
agents
managing
IPF,
offering
new
avenue
targets
core
inflammatory
processes
this
debilitating
condition.
Graphical
Drug Development and Industrial Pharmacy,
Год журнала:
2025,
Номер
unknown, С. 1 - 18
Опубликована: Фев. 18, 2025
Objective
This
review
aims
to
explore
innovative
therapeutic
strategies,
with
a
particular
focus
on
recent
advancements
in
drug
delivery
systems
using
bioinspired
nanomaterials
such
as
solid
lipid
nanoparticles
(SLNs)
and
nanostructured
carriers
(NLCs)
for
the
Idiopathic
pulmonary
fibrosis
(IPF).
Radiation-induced
tissue
injury
(RITI)
is
the
most
common
complication
in
clinical
tumor
radiotherapy.
Due
to
heterogeneity
response
of
different
tissues
radiation
(IR),
radiotherapy
will
cause
types
and
degrees
RITI,
which
greatly
limits
application
Efforts
are
continuously
ongoing
elucidate
molecular
mechanism
RITI
develop
corresponding
prevention
treatment
drugs
for
RITI.
Single-cell
sequencing
(Sc-seq)
has
emerged
as
a
powerful
tool
uncovering
mechanisms
identifying
potential
targets
by
enhancing
our
understanding
complex
intercellular
relationships,
facilitating
identification
novel
cell
phenotypes,
allowing
assessment
spatiotemporal
developmental
trajectories.
Based
on
comprehensive
review
we
analyzed
regulatory
networks
combination
with
Sc-seq
summarized
targeted
intervention
pathways
therapeutic
Deciphering
diverse
underlying
can
shed
light
its
pathogenesis
unveil
new
avenues
potentially
facilitate
repair
or
regeneration
currently
irreversible
Furthermore,
discuss
how
personalized
strategies
based
offer
promise
mitigating
International Journal of Molecular Sciences,
Год журнала:
2025,
Номер
26(2), С. 517 - 517
Опубликована: Янв. 9, 2025
Following
the
COVID-19
pandemic,
prevalence
of
pulmonary
fibrosis
has
increased
significantly,
placing
patients
at
higher
risk
and
presenting
new
therapeutic
challenges.
Current
anti-fibrotic
drugs,
such
as
Nintedanib,
can
slow
decline
in
lung
function,
but
their
severe
side
effects
highlight
urgent
need
for
safer
more
targeted
alternatives.
This
study
explores
potential
underlying
mechanisms
an
endogenous
peptide
(P5)
derived
from
fibroblast
growth
factor
2
(FGF2),
developed
by
our
research
team.
Using
a
bleomycin-induced
mouse
model,
we
observed
that
P5
alleviated
inhibiting
collagen
deposition,
confirmed
CT
scans
histological
staining.
In
TGF-β-induced
cell
models,
effectively
suppressed
deposition
epithelial–mesenchymal
transition
(EMT).
Transcriptome
analysis
highlighted
pathways
related
to
receptor
binding,
extracellular
matrix
organization,
adhesion,
with
KEGG
confirming
FGFR/MAPK
signaling
inhibition
primary
mechanism
its
effects.
summary,
demonstrates
significantly
attenuates
through
EMT,
signaling,
providing
promising
approach
fibrosis.
BMJ Case Reports,
Год журнала:
2025,
Номер
18(3), С. e263966 - e263966
Опубликована: Март 1, 2025
Idiopathic
pulmonary
fibrosis
(IPF)
is
a
fibrosing
pneumonia
of
unknown
causation
with
chronic,
progressive
course
that
may
be
modified
by
treatment
the
antifibrotic
agents,
pirfenidone
and
nintedanib.
Both
drugs
have
been
shown
to
slow
disease
progression,
but,
in
rare
cases,
has
stabilise
even
improve
lung
function.
We
present
case
patient
whose
function
pathognomonic
features
on
CT
imaging
improved
significantly
commencement
pirfenidone.
Withholding
was
associated
functional
morphological
deterioration
subsequently
reversed
stabilised
following
recommencement
this
treatment.
discuss
potential
mechanisms
might
explain
response,
compare
our
others
described
previously
consequences
restricted
prescribing
within
specified
range
vital
capacity
opportunity
influence
natural
history
IPF
early
before
irreversible
develops.
Frontiers in Endocrinology,
Год журнала:
2025,
Номер
16
Опубликована: Март 20, 2025
Tissue
fibrosis
represents
an
aberrant
repair
process,
occurring
because
of
prolonged
injury,
sustained
inflammatory
response,
or
metabolic
disorders.
It
is
characterized
by
excessive
accumulation
extracellular
matrix
(ECM),
resulting
in
tissue
hardening,
structural
remodeling,
and
loss
function.
This
pathological
phenomenon
a
common
feature
the
end
stage
numerous
chronic
diseases.
Despite
advent
novel
therapeutic
modalities,
including
antifibrotic
agents,
these
have
only
modest
efficacy
reversing
established
are
associated
with
adverse
effects.
In
recent
years,
growing
body
research
has
demonstrated
that
exercise
significant
benefits
potential
treatment
fibrosis.
The
anti-fibrotic
effects
mediated
multiple
mechanisms,
direct
inhibition
fibroblast
activation,
reduction
expression
pro-fibrotic
factors
such
as
transforming
growth
factor-β
(TGF-β)
slowing
collagen
deposition.
Furthermore,
been
to
assist
maintaining
dynamic
equilibrium
repair,
thereby
indirectly
reducing
damage
can
also
help
maintain
balance
improving
disorders,
exerting
anti-inflammatory
antioxidant
effects,
regulating
cellular
autophagy,
restoring
mitochondrial
function,
activating
stem
cell
activity,
apoptosis,
alleviating
tissue.
paper
presents
review
its
underlying
mechanisms
for
range
fibrosis,
cardiac,
pulmonary,
renal,
hepatic,
skeletal
muscle.
offers
valuable
reference
point
non-pharmacological
intervention
strategies
comprehensive
fibrotic
Journal of Medicinal Chemistry,
Год журнала:
2024,
Номер
unknown
Опубликована: Сен. 20, 2024
Idiopathic
pulmonary
fibrosis
(IPF)
is
a
progressive
and
lethal
lung
disease
with
an
elusive
etiology.
Aberrant
activation
of
c-Jun
N-terminal
kinase
1
(JNK1)
has
been
implicated
in
its
pathogenesis.
Through
combination
structure-based
drug
design
structure-activity
relationship
(SAR)
optimization,
series
pyrimidine-2,4-diamine
scaffold
derivatives
have
developed
as
potent
JNK1
inhibitors.
Compound