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
Frontiers in Medicine,
Год журнала:
2024,
Номер
11
Опубликована: Март 25, 2024
Excessive
accumulation
of
extracellular
matrix
(ECM)
components
within
the
liver
leads
to
a
pathological
condition
known
as
fibrosis.
Alcohol
abuse,
non-alcoholic
fatty
disease
(NAFLD),
autoimmune
issues,
and
viral
hepatitis
cause
chronic
injury.
Exploring
potential
therapeutic
targets
understanding
molecular
mechanisms
involved
in
fibrosis
are
essential
for
development
effective
interventions.
The
goal
this
comprehensive
review
is
explain
how
PI3K/AKT
signaling
pathway
contributes
reduction
target
investigated
through
summary
results
from
vivo
vitro
studies.
Studies
focusing
on
activation
have
shown
significant
decrease
markers
improvement
function.
emphasizes
may
prevent
ECM
synthesis
hepatic
stellate
cell
(HSC)
activation,
ultimately
reducing
fibrotic
response.
specific
downstream
effectors
constitute
rapidly
developing
field
study.
In
conclusion,
plays
role
attenuating
Its
complex
regulating
HSC
production,
demonstrated
both
,
underscores
its
approach
managing
slowing
progression.
A
provides
valuable
insights
into
future
developments
implications
clinical
applications.
Liver
fibrosis
is
a
very
complicated
dynamic
process
where
several
immune
cells
are
involved.
Both
innate
and
adaptive
immunity
implicated,
their
interplay
always
present.
Multi-directional
interactions
between
liver
macrophages,
hepatic
stellate
(HSCs),
cells,
cytokines
important
for
the
induction
perpetuation
of
fibrosis.
Detailed
studies
proteomics
transcriptomics
have
produced
new
evidence
role
individual
in
cirrhosis.
Most
these
controlled
by
various
checkpoints
whose
main
function
to
maintain
homeostasis
implicated
cells.
Recent
indicates
that
involved
In
particular,
programmed
cell
death
protein
1
(PD-1),
death-ligand
(PD-L1),
cytotoxic
T
lymphocyte-associated
antigen
4
(CTLA-4)
been
investigated,
particularly
after
availability
checkpoint
inhibitors.
Their
activation
leads
exhaustion
CD4+ve
CD8+ve
promotion
this
review,
current
pathogenesis
immunological
abnormalities
discussed.
The
recent
data
on
involvement
identified
as
possible
targets
future
interventions.
Pharmacological Research,
Год журнала:
2024,
Номер
203, С. 107155 - 107155
Опубликована: Март 23, 2024
Non-alcoholic
fatty
liver
disease
(NAFLD)
encompasses
hepatic
steatosis,
non-alcoholic
steatohepatitis
(NASH),
fibrosis,
cirrhosis,
and
hepatocellular
carcinoma.
It
is
the
primary
cause
of
chronic
disorders,
with
a
high
prevalence
but
no
approved
treatment.
Therefore,
it
indispensable
to
find
trustworthy
therapy
for
NAFLD.
Recently,
mounting
evidence
illustrates
that
Sirtuin
1
(SIRT1)
strongly
associated
SIRT1
activation
or
overexpression
attenuate
NAFLD,
while
deficiency
aggravates
Besides,
an
array
therapeutic
agents,
including
natural
compounds,
synthetic
traditional
Chinese
medicine
formula,
stem
cell
transplantation,
alleviates
NALFD
via
upregulation.
Mechanically,
NAFLD
by
reestablishing
autophagy,
enhancing
mitochondrial
function,
suppressing
oxidative
stress,
coordinating
lipid
metabolism,
as
well
reducing
hepatocyte
apoptosis
inflammation.
In
this
review,
we
introduced
structure
function
briefly,
summarized
effect
on
its
mechanism,
along
application
agonists
in
treating
Frontiers in Immunology,
Год журнала:
2023,
Номер
14
Опубликована: Май 19, 2023
Fibrosis
is
a
pathological
tissue
repair
activity
in
which
many
myofibroblasts
are
activated
and
extracellular
matrix
excessively
accumulated,
leading
to
the
formation
of
permanent
scars
finally
organ
failure.
A
variety
organs,
including
lung,
liver,
kidney,
heart,
skin,
can
undergo
fibrosis
under
stimulation
various
exogenous
or
endogenous
pathogenic
factors.
At
present,
pathogenesis
still
not
fully
elucidated,
but
it
known
that
immune
system
plays
key
role
initiation
progression
fibrosis.
Immune
checkpoint
molecules
regulators
maintain
tolerance
homeostasis,
among
programmed
cell
death
protein
1/programmed
ligand
1
(PD-1/PD-L1)
axis
has
attracted
much
attention.
The
exciting
achievements
tumor
immunotherapy
targeting
PD-1/PD-L1
provide
new
insights
into
its
use
as
therapeutic
target
for
other
diseases.
In
recent
years,
been
preliminarily
explored,
further
confirming
close
relationship
signaling,
regulation,
This
review
discusses
structure,
expression,
function,
regulatory
mechanism
PD-1
PD-L1,
summarizes
research
progress
signaling
fibrotic
Environmental Toxicology,
Год журнала:
2024,
Номер
39(5), С. 2487 - 2501
Опубликована: Янв. 4, 2024
Abstract
Recent
studies
have
shown
that
chondrocyte
ferroptosis
contributes
importantly
to
the
pathogenesis
of
osteoarthritis
(OA).
However,
it
is
largely
unknown
how
regulated.
In
this
study,
data
sets
GSE167852
and
GSE190184
were
downloaded
from
Gene
Expression
Omnibus
(GEO)
database,
161
differentially
expressed
genes
(DEGs)
related
screened
by
bioinformatics
analysis.
Subsequently,
ADORA2B
was
as
a
candidate
gene
DEGs,
which
significantly
upregulated
in
palmitic
acid
(PA)
treated
chondrocytes.
CCK‐8,
EdU,
Western
blotting,
ferroptosis‐related
kits
assays
demonstrated
knockdown
constrained
promoted
viability
Overexpression
ferroptosis,
while
PI3K/Akt
pathway
inhibitor
LY294002
reversed
promotion
on
ferroptosis.
Dual‐luciferase
reporter
assay
chromatin
immunoprecipitation
(ChIP)
indicated
MYC
transcription
suppressor
ADORA2B,
overexpression
viability,
inhibited
chondrocytes,
abated
inhibition
vivo
experiments
showed
alleviated
cartilage
tissue
damage
OA
mice,
able
overexpression.
summary,
transcriptionally
suppressing
MYC,
promotes
chondrocytes
via
pathway.
Thus,
can
be
used
potential
treatment
target
for
diseases.
Frontiers in Endocrinology,
Год журнала:
2023,
Номер
14
Опубликована: Окт. 10, 2023
Inflammatory
bowel
disease
(IBD)
has
been
referred
to
as
the
“green
cancer,”
and
its
progression
colorectal
cancer
(CRC)
poses
a
significant
challenge
for
medical
community.
A
common
factor
in
their
development
is
glycolysis,
crucial
metabolic
mechanism
of
living
organisms,
which
also
involved
other
diseases.
In
IBD,
glycolysis
affects
gastrointestinal
components
such
intestinal
microbiota,
mucosal
barrier
function,
immune
system,
including
macrophages,
dendritic
cells,
T
neutrophils,
while
CRC,
it
linked
various
pathways,
phosphatidylinositol-3-kinase
(PI3K)/AKT,
AMP-activated
protein
kinase
(AMPK),
mammalian
target
rapamycin
(mTOR),
transcription
factors
p53,
Hypoxia-inducible
(HIF),
c-Myc.
Thus,
comprehensive
study
essential
better
understanding
pathogenesis
therapeutic
targets
both
IBD
CRC.
This
paper
reviews
role
diseases,
particularly
via
effects
on
immunity,
integrity,
signaling
some
strategies
targeting
glycolytic
enzymes.
