Molecular Biology Reports,
Год журнала:
2024,
Номер
51(1)
Опубликована: Апрель 15, 2024
Abstract
Background
Atrial
Fibrillation
(AF),
a
prevalent
arrhythmic
condition,
is
intricately
associated
with
atrial
fibrosis,
major
pathological
contributor.
Central
to
the
development
of
fibrosis
myocardial
inflammation.
This
study
focuses
on
Natriuretic
Peptide
(ANP)
and
its
role
in
mitigating
aiming
elucidate
specific
mechanisms
by
which
ANP
exerts
effects,
an
emphasis
fibroblast
dynamics.
Methods
results
The
involved
forty
Sprague-Dawley
rats,
divided
into
four
groups:
control,
Angiotensin
II
(Ang
II),
Ang
+
ANP,
only.
administration
1
µg/kg/min
was
given
groups,
while
both
groups
received
0.1
intravenously
for
duration
14
days.
Cardiac
fibroblasts
were
used
vitro
validation
proposed
mechanisms.
observed
that
rats
showed
increase
blood
pressure
decrease
body
weight,
more
pronounced
group.
Diastolic
dysfunction,
characteristic
group,
alleviated
ANP.
Additionally,
significantly
reduced
II-induced
myofibroblast
proliferation,
collagen
overexpression,
macrophage
infiltration,
elevated
expression
Interleukin
6
(IL-6)
Tenascin-C
(TN-C).
Transcriptomic
sequencing
indicated
enhanced
PI3K/Akt
signaling
Furthermore,
studies
along
PI3K
inhibitor
LY294002,
effectively
pathway
activation
TN-C,
collagen-I,
collagen-III,
induced
II.
Conclusions
demonstrates
ANP’s
potential
inhibiting
inflammation
reducing
fibrosis.
Notably,
effect
countering
seems
be
mediated
through
suppression
PI3K/Akt-Tenascin-C
pathway.
These
insights
enhance
our
understanding
AF
pathogenesis
position
as
therapeutic
agent
treating
Advanced Science,
Год журнала:
2025,
Номер
unknown
Опубликована: Май 20, 2025
Abstract
Fibrosis,
characterized
by
abnormal
deposition
of
structural
proteins,
is
a
major
cause
tissue
dysfunction
in
chronic
diseases.
The
disease
burden
associated
with
progressive
fibrosis
substantial,
and
currently
approved
drugs
are
unable
to
effectively
reverse
it.
Immune
cells
increasingly
recognized
as
crucial
regulators
the
pathological
process
releasing
effector
molecules,
such
cytokines,
chemokines,
extracellular
vesicles,
metabolites,
proteases,
or
intercellular
contact.
Therefore,
targeting
immune
microenvironment
can
be
potential
strategy
for
reduction
reversion.
This
review
summarizes
recent
advances
understanding
including
phenotypic
functional
transformations
interaction
other
cells.
novel
opportunities
discovery
development
remodeling
their
challenges
also
discussed.
Frontiers in Pharmacology,
Год журнала:
2022,
Номер
13
Опубликована: Окт. 4, 2022
Extensive
research
has
implicated
inflammation
and
oxidative
stress
in
the
development
of
multiple
diseases,
such
as
diabetes,
hepatitis,
arthritis.
Kinsenoside
(KD),
a
bioactive
glycoside
component
extracted
from
medicinal
plant
Anoectochilus
roxburghii
,
been
shown
to
exhibit
potent
anti-inflammatory
anti-oxidative
abilities.
In
this
review,
we
summarize
effects
KD,
including
hepatoprotection,
pro-osteogenesis,
anti-hyperglycemia,
vascular
protection,
immune
regulation,
vision
infection
inhibition,
which
are
partly
responsible
for
suppressing
signaling
stress.
The
protective
action
KD
against
dysfunctional
lipid
metabolism
is
also
associated
with
limiting
inflammatory
signals,
due
crosstalk
between
metabolism.
Ferroptosis,
process
involved
both
damage,
potentially
regulated
by
KD.
addition,
discuss
physicochemical
properties
pharmacokinetic
profiles
Advances
cultivation
artificial
synthesis
techniques
promising
evidence
that
shortage
raw
materials
required
production
can
be
overcome.
novel
drug
delivery
systems
improve
vivo
rapid
clearance
poor
bioavailability
integrated
aim
offer
insights
into
molecular
mechanisms
underlying
therapeutic
role
lay
solid
foundations
utilization
clinical
practice.
Molecular Biology Reports,
Год журнала:
2024,
Номер
51(1)
Опубликована: Апрель 15, 2024
Abstract
Background
Atrial
Fibrillation
(AF),
a
prevalent
arrhythmic
condition,
is
intricately
associated
with
atrial
fibrosis,
major
pathological
contributor.
Central
to
the
development
of
fibrosis
myocardial
inflammation.
This
study
focuses
on
Natriuretic
Peptide
(ANP)
and
its
role
in
mitigating
aiming
elucidate
specific
mechanisms
by
which
ANP
exerts
effects,
an
emphasis
fibroblast
dynamics.
Methods
results
The
involved
forty
Sprague-Dawley
rats,
divided
into
four
groups:
control,
Angiotensin
II
(Ang
II),
Ang
+
ANP,
only.
administration
1
µg/kg/min
was
given
groups,
while
both
groups
received
0.1
intravenously
for
duration
14
days.
Cardiac
fibroblasts
were
used
vitro
validation
proposed
mechanisms.
observed
that
rats
showed
increase
blood
pressure
decrease
body
weight,
more
pronounced
group.
Diastolic
dysfunction,
characteristic
group,
alleviated
ANP.
Additionally,
significantly
reduced
II-induced
myofibroblast
proliferation,
collagen
overexpression,
macrophage
infiltration,
elevated
expression
Interleukin
6
(IL-6)
Tenascin-C
(TN-C).
Transcriptomic
sequencing
indicated
enhanced
PI3K/Akt
signaling
Furthermore,
studies
along
PI3K
inhibitor
LY294002,
effectively
pathway
activation
TN-C,
collagen-I,
collagen-III,
induced
II.
Conclusions
demonstrates
ANP’s
potential
inhibiting
inflammation
reducing
fibrosis.
Notably,
effect
countering
seems
be
mediated
through
suppression
PI3K/Akt-Tenascin-C
pathway.
These
insights
enhance
our
understanding
AF
pathogenesis
position
as
therapeutic
agent
treating
