Frontiers in Bioengineering and Biotechnology,
Journal Year:
2025,
Volume and Issue:
12
Published: Jan. 8, 2025
Myocardial
infarction
(MI)
is
the
leading
cause
of
morbidity
and
mortality
worldwide.
Curcumin
has
been
observed
to
significantly
reduce
pathological
processes
associated
with
MI.
Its
clinical
application
limited
due
its
low
bioavailability,
rapid
degradation,
poor
solubility.
Advancements
in
nanotechnology
can
be
used
enhance
therapeutic
potentials
nano-formulation
enhances
solubility,
stability,
allowing
more
precise
delivery
ischemic
cardiac
tissue.
nanoparticles
have
successfully
infarct
size,
maintain
heart
function
by
modulating
essential
molecular
pathways
liposomal
formulations
provide
sustained
release
higher
tissue
penetration
improved
pharmacokinetics
enhanced
efficacy.
Preclinical
studies
revealed
that
nanocurcumin
drastically
lower
oxidative
stress
indicators,
inflammatory
cytokines,
damage.
Micelles
composed
polymers
demonstrated
high
biocompatibility
targeting
capabilities
increased
cardio-protective
effects.
Research
trials
are
for
comprehensive
analysis
efficacy
curcumin-based
nano-therapeutics
cardiovascular
condition
lowering
risk
Cell Death Discovery,
Journal Year:
2025,
Volume and Issue:
11(1)
Published: Feb. 17, 2025
Abstract
Spleen
tyrosine
kinase
(Syk),
an
important
hub
of
immune
signaling,
is
activated
by
several
signalings
in
active
lupus
which
could
be
interfered
Syk
inhibitor
but
still
not
completely
evaluated
innate
cells
associated
with
activity.
Hence,
a
(fostamatinib;
R788)
was
tested
vivo
using
Fc
gamma
receptor-deficient
(FcγRIIb
−/−
)
mice
and
vitro
(macrophages
neutrophils).
After
4
weeks
oral
inhibitor,
40
week-old
FcγRIIb
(a
full-blown
model)
demonstrated
less
prominent
parameters
(serum
anti-dsDNA,
proteinuria,
glomerulonephritis),
systemic
inflammation,
as
serum
TNFa,
IL-6,
citrullinated
histone
H3
(CitH3),
gut
permeability
defect,
indicated
FITC
dextran
assay,
lipopolysaccharide
(LPS),
(1
→
3)-β-D-glucan
(BG),
extracellular
traps
(ETs)
complex
deposition
spleens
kidneys
(immunofluorescent
staining
CitH3
immunoglobulin
G)
than
placebo.
Due
to
the
spontaneous
elevation
LPS
BG
serum,
plus
(LPS
+
BG)
used
activate
macrophages
neutrophils.
stimulation,
neutrophils
predominant
abundance
phosphorylated
(Western
blotting),
pro-inflammatory
responses
(CD86
flow
cytometry
analysis,
supernatant
cytokines,
ETs
immunofluorescent,
cytometry-based
apoptosis).
With
RNA
sequencing
analysis
western
blotting,
Syk-p38MAPK-dependent
pathway
suggested
downregulating
inflammatory
pathways
BG-activated
Although
both
inhibitors
against
p38MAPK
attenuated
macrophage
neutrophil
WGP,
apoptosis
inhibition
observed.
These
results
that
(fostamatinib)
improved
severity
caused
defect
partly
through
Syk-p38MAPK
anti-inflammation
inhibited
ET
formation
cytokine
production
from
cells.
Frontiers in Cell and Developmental Biology,
Journal Year:
2025,
Volume and Issue:
13
Published: March 10, 2025
The
mammalian
p38
MAPK
pathway
plays
a
vital
role
in
transducing
extracellular
environmental
stresses
into
numerous
intracellular
biological
processes.
have
been
linked
to
variety
of
cellular
processes
including
inflammation,
cell
cycle,
apoptosis,
development
and
tumorigenesis
specific
types.
has
implicated
the
many
human
diseases
become
target
for
treatment
cancer.
Although
extensively
studied,
questions
still
await
clarification.
More
comprehensive
understanding
will
provide
new
possibilities
diseases.
Hog1
S.
cerevisiae
is
conserved
homolog
cells
HOG
signaling
studied.
deep
help
clues
clarifying
pathway,
thereby
furthering
our
relationship
between
disease.
In
this
review,
we
elaborate
functions
while
also
analyzing
how
regulates
response
stresses.
1,
various
cells.2,
health.3,
as
Saccharomyces
.
cells.
2,
health.
3,
ACS Infectious Diseases,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 14, 2025
The
integration
of
RNA-
and
DNA-based
assays
enables
the
investigation
disease
dynamics,
specifically
assessing
role
asymptomatic
or
subclinical
infections
in
malaria
transmission.
Circular
RNAs
(circRNAs),
a
distinct
category
noncoding
RNAs,
are
implicated
numerous
pathogenic
mechanisms.
As
now,
research
has
yet
to
explore
circRNAs'
function
infection.
findings
revealed
that
Plasmodium
infection
upregulated
60
circRNAs
downregulated
71
BALB/c
mice.
We
selected
11
differentially
expressed
(DE)
according
prediction
target
miRNA-mRNA
coding
protein,
these
were
further
confirmed
by
validation
experiments.
IRESfinder,
GO,
KEGG
evaluations
indicated
7
DE
possess
protein-coding
potential
enriched
MAPK
signaling
cascade.
In
P.y17XL-infected
mouse
models,
substantiated
dynamic
characteristics
correlated
with
inflammation,
NF-κB
cascades
activated,
also
contributing
inflammatory
reaction
during
This
study
establishes
Plasmodium-induced
circRNA
expression
as
novel
mechanism
which
parasite
modulates
host
immune
signaling,
advancing
understanding
Plasmodium–host
cell
interactions.
addition,
42
found
normal
mice,
25
discovered
excluding
1238
shared
changes
profile
host,
altered
involved
response
possibly
regulates
reverse
splicing
pre-mRNA
m6A
modification
RNA,
inducing
production
host.
Biomedicines,
Journal Year:
2025,
Volume and Issue:
13(4), P. 802 - 802
Published: March 27, 2025
Background:
Gut
barrier
integrity
plays
a
crucial
role
in
the
pathogenesis
of
metabolic
dysfunction-associated
fatty
liver
disease
(MAFLD).
Electroacupuncture
(EA)
at
ST-36
can
ameliorate
inflammatory
responses
via
stimulating
α7
nicotinic
acetylcholine
receptor
(α7nAChR),
but
whether
EA
is
effective
preserving
intestinal
MAFLD
has
not
been
exactly
illustrated.
This
investigation
explored
potential
protection
mechanisms
targeting
dismantled
gut
MAFLD.
Methods:
C57BL/6
mice
were
randomly
allocated
into
several
subgroups:
control
(CON),
high-fat
diet
(HFD),
HFD
with
EA,
and
α7nAChR
inhibitor
α-BGT,
HO-1
knockout
(KO).
Body
weight,
visceral
fat
index,
histopathological
examination
intestine
determined.
Serum
biological
indexes
evaluated
through
corresponding
kits.
Furthermore,
expressions
HO-1,
α7nAChR,
barrier-associated
proteins,
molecular
tissues
assessed
Western
blot,
RT-qPCR,
immunohistology,
or
immunofluorescence
examination.
Results:
treatment
decreased
body
index
gain
mitigated
function
injury
abnormal
lipid
indexes,
exhibiting
less
severity
hepatic
steatosis,
fibrosis,
inflammation
Lower
permeability,
epithelial
disruption,
upregulation
tight
junction
proteins
after
suggested
protective
effects
attenuating
dysfunction.
These
abolished
by
α-BGT
deletion.
Mechanistically,
markedly
enriched
expression
phosphorylated
p38
MAPK/NF-κB
activation,
which
was
lost
KO
treatment.
Conclusions:
The
may
be
attributed
to
preserved
barrier,
thereby
alleviating
systemic
preventing
subsequent
hits,
where
α7nAChR-mediated
HO-1/p38
pathway
maintain
homeostasis.
