Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
15
Published: Oct. 18, 2024
Background
Prostate
cancer
is
one
of
the
leading
causes
cancer-related
deaths
in
men.
Its
molecular
pathogenesis
closely
linked
to
various
genetic
and
epigenetic
alterations,
including
posttranslational
modifications
like
SUMOylation.
Identifying
biomarkers
that
predict
outcomes
specific
therapeutic
targets
depends
on
a
comprehensive
understanding
these
processes.
With
growing
interest
SUMOylation
as
mechanism
affecting
prostate
genes,
this
study
aimed
investigate
central
role
prognostics,
focusing
significance
NOP58.
Methods
We
conducted
bioinformatics
analysis,
integrating
differential
expression
survival
gene
set
enrichment
analysis
(GSEA),
single-cell
transcriptomic
analyses
using
data
from
The
Cancer
Genome
Atlas
(TCGA).
Key
genes
were
identified
through
intersections
Venn
diagrams,
Boralta
algorithm
signatures,
machine
learning
models.
These
signaling
mechanisms
validated
experimental
studies,
immunohistochemical
staining
ontology
analyses.
Results
dual-gene
subtype
with
SUMO1,
SUMO2,
XPO1
revealed
significant
differences
across
subtypes,
further
emphasizing
potential
impact
NOP58
SUMOylation,
key
post-translational
modification,
cancer.
overexpression
was
strongly
associated
shorter
overall
(OS),
progression-free
interval
(PFI),
disease-specific
death
patients.
Immunohistochemical
confirmed
significantly
overexpressed
tissues
compared
normal
tissues.
ROC
curve
demonstrated
could
distinguish
control
samples
high
diagnostic
accuracy.
Gene
Ontology
along
GSVA
GSEA,
suggested
may
be
involved
cell
cycle
regulation
DNA
repair
pathways.
Moreover,
knockdown
led
increased
BCL2
decreased
Ki67
levels,
promoting
apoptosis
inhibiting
proliferation.
Colony
formation
assays
showed
inhibited,
while
its
promoted,
colony
formation,
highlighting
critical
growth
survival.
Additionally,
drug
responses,
Methotrexate,
Rapamycin,
Sorafenib,
Vorinostat.
Conclusion
regulator
progression
mediation
pathway.
level
serves
reliable
prognostic
biomarker
an
actionable
target,
advancing
precision
medicine
for
Targeting
enhance
efficacy
improve
oncology.
IJC Heart & Vasculature,
Journal Year:
2024,
Volume and Issue:
53, P. 101469 - 101469
Published: July 23, 2024
Sphingolipids
are
eighteen
carbon
alcohol
lipids
synthesized
from
non-sphingolipid
precursors
in
the
endoplasmic
reticulum
(ER).
The
sphingolipids
serve
as
for
a
vast
range
of
moieties
found
our
cells
that
play
critical
role
various
cellular
processes,
including
cell
division,
senescence,
migration,
differentiation,
apoptosis,
pyroptosis,
autophagy,
nutrition
intake,
metabolism,
and
protein
synthesis.
In
CVDs,
different
subclasses
other
derived
molecules
such
sphingomyelin
(SM),
ceramides
(CERs),
sphingosine-1-phosphate
(S1P)
directly
related
to
diabetic
cardiomyopathy,
dilated
myocarditis,
ischemic
heart
disease
(IHD),
hypertension,
atherogenesis.
Several
genome-wide
association
studies
showed
an
between
genetic
variations
sphingolipid
pathway
genes
risk
CVDs.
plays
important
biogenesis
secretion
exosomes.
Small
extracellular
vesicles
(sEVs)/
exosomes
have
recently
been
possible
indicators
onset
linking
signaling
pathways
contribute
progression.
Important
features
EVs
like
biocompatibility,
crossing
biological
barriers
can
improve
pharmacokinetics
drugs
will
be
exploited
develop
next-generation
drug
delivery
systems.
this
review,
we
comprehensively
discussed
sphingolipids,
metabolites
development
addition,
concise
deliberations
were
laid
discuss
sEVs/exosomes
regulating
pathophysiological
processes
CVDs
therapeutic
targets.
Current Treatment Options in Cardiovascular Medicine,
Journal Year:
2025,
Volume and Issue:
27(1)
Published: April 9, 2025
In
recent
years,
several
pre-clinical
studies
have
demonstrated
the
therapeutic
potential
of
stem
cell-derived
exosomes
in
treatment
cardiovascular
disease
(CVD).
Here,
we
evaluate
their
as
biomarkers
for
detection
and
monitoring
CVD,
with
a
particular
focus
on
pediatric
heart
disease.
Exosomes
isolated
from
cell
sources,
including
mesenchymal
cells
(MSCs)
pluripotent
(PSCs),
benefit
function,
inflammatory
responses,
angiogenesis
injured
diseased
hearts.
These
carry
variety
cargo,
such
proteins,
lipids,
nucleic
acids.
However,
majority
contain
non-coding
RNA
molecules.
Review
existing
literature
RNAs
relationship
to
CVD
suggests
that
containing
microRNAs
(miRNAs)
can
serve
promising
due
presence
circulation,
ease
isolation,
potential.
are
especially
screening
diagnostic
tools
early
congenital
Bioengineering,
Journal Year:
2025,
Volume and Issue:
12(2), P. 205 - 205
Published: Feb. 19, 2025
Myocardial
infarction
(MI)
is
a
cardiovascular
disease
(CVD)
with
high
morbidity
and
mortality
worldwide,
which
serious
threat
to
human
life
health.
Inflammatory
immune
responses
are
initiated
immediately
after
MI,
unbalanced
inflammation
post-MI
can
lead
cardiac
dysfunction,
scarring,
ventricular
remodeling,
emphasizing
the
critical
need
for
an
effective
inflammation-regulating
treatment.
With
development
of
novel
therapies,
drug
delivery
system
specific
inflammatory
cells
offers
significant
potential.
In
this
review,
we
introduce
fibroblasts
involved
in
MI
summarize
newly
developed
systems
related
use
injectable
hydrogels,
patches,
nanoparticles,
extracellular
vesicles
(EVs).
Finally,
highlight
recent
trends
cell-targeting
involving
different
strategies
that
facilitate
treatment
MI.
Journal of Nanobiotechnology,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: April 23, 2025
Endogenous
neurogenesis
could
promote
stroke
recovery.
Furthermore,
anti-inflammatory
phenotypical
microglia
(M2-microglia)
facilitate
Neural
Stem
Cell
(NSC)-mediated
following
Ischemic
Stroke
(IS).
Nonetheless,
the
mechanisms
through
which
M2
influence
NSC-mediated
post-IS
remain
unclear.
On
other
hand,
microglia-derived
small
Extracellular
Vesicles
(M2-sEVs)
exert
phenomenal
biological
effects
and
play
significant
roles
in
cell-to-cell
interactions,
highlighting
their
potential
involvement
post-IS,
forming
basis
of
this
study.
M2-sEVs
were
first
isolated
from
IL-4-stimulated
microglia.
For
vivo
tests,
intravenously
injected
into
mice
every
day
for
14
days
after
transient
Middle
Cerebral
Artery
Occlusion
(tMCAO).
Following
that,
infarct
volume
neurological
function,
as
well
NSC
proliferation
Subventricular
Zone
dentate
gyrus,
migration,
differentiation
area,
examined.
vitro
administered
to
subjected
Oxygen-Glucose
Deprivation
(OGD)
then
reoxygenation,
assessed.
Finally,
microRNA
sequencing
explore
regulatory
mechanisms.
Our
findings
revealed
that
reduced
increased
score
post-tMCAO.
M2-sEV
treatment
promoted
neuronal
both
vitro.
Additionally,
miR-93-5p
miR-25-3p
enrichment
M2-sEVs.
Inhibitors
these
miRNAs
prevented
TGFBR,
PTEN,
FOXO3
downregulation
NSC,
reversing
M2-sEVs'
beneficial
on
sensorimotor
differentiation,
protected
against
IS,
at
least
partially,
via
delivering
downregulate
expression
NSC.
Frontiers in Immunology,
Journal Year:
2025,
Volume and Issue:
16
Published: May 8, 2025
Myocardial
infarction
(MI),
which
is
characterized
by
high
morbidity
and
mortality,
a
serious
threat
to
human
life
health,
timely
reperfusion
therapy
save
ischemic
myocardium
currently
the
most
effective
intervention.
Although
effectively
restores
coronary
blood
flow
maximally
limits
infarct
size,
it
triggers
additional
cell
death
tissue
damage,
known
as
myocardial
ischemia/reperfusion
injury
(MIRI).
Multiple
immune
cells
are
present
in
area,
executing
specific
functions
engaging
crosstalk
during
diverse
stages,
constituting
complex
microenvironment
involved
repair
regeneration
after
MIRI.
Immunotherapy
brings
new
hope
for
treating
heart
disease
modulating
microenvironment.
In
this
paper,
we
explore
regulatory
roles
of
various
MIRI
close
relationship
between
different
deaths
addition,
current
status
research
on
targeting
system
intervene
MIRI,
with
expectation
providing
basis
achieving
clinical
translation.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Dec. 2, 2024
Heart
failure
(HF)
is
a
complex
and
debilitating
condition
characterized
by
the
heart's
inability
to
pump
blood
effectively,
leading
significant
morbidity
mortality.
The
abnormality
of
immune
response
key
factor
in
progression
HF,
contributing
adverse
cardiac
remodeling
dysfunction.
Exosomal
microRNAs
(miRNAs)
play
pivotal
role
regulating
gene
expression
cellular
function,
which
are
integral
crosstalk
between
cells,
influencing
cell
functions,
such
as
macrophage
polarization,
T
activity,
cytokine
production,
thereby
modulating
various
pathological
processes
inflammation,
fibrosis,
This
review
emphasizes
immune-regulatory
exosomal
miRNAs
HF
highlights
their
clinical
potential
diagnostic
biomarkers
therapeutic
agents.