bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2023,
Volume and Issue:
unknown
Published: Aug. 5, 2023
Abstract
Sepsis
is
the
leading
systemic
inflammatory
response
syndrome
in
worldwide,
yet
relatively
little
known
about
genes
and
signaling
pathways
involved
sepsis
progression.
The
current
investigation
aimed
to
elucidate
potential
key
candidate
its
associated
complications.
Next
generation
sequencing
(NGS)
dataset
(GSE185263)
was
downloaded
from
Gene
Expression
Omnibus
(GEO)
database,
which
included
data
348
samples
44
normal
control
samples.
Differentially
expressed
(DEGs)
were
identified
using
t-tests
DESeq2
R
package.
Next,
we
made
use
of
g:Profiler
analyze
gene
ontology
(GO)
REACTOME
pathway.
Then
protein-protein
interaction
(PPI)
these
DEGs
visualized
by
Cytoscape
with
Search
Tool
for
Retrieval
Interacting
Genes
(STRING).
Furthermore,
constructed
miRNA-hub
regulatory
network
TF-hub
among
hub
utilizing
miRNet
NetworkAnalyst
online
databases
tool
software.
Finally,
performed
receiver
operating
characteristic
(ROC)
curve
analysis
through
pROC
package
statistical
In
total,
958
identified,
479
up
regulated
down
regulated.
GO
results
showed
that
mainly
enriched
regulation
cellular
process,
stimulus,
extracellular
matrix
organization
immune
system.
PRKN,
KIT,
FGFR2,
GATA3,
ERBB3,
CDK1,
PPARG,
H2BC5,
H4C4
CDC20
might
be
Predicted
miRNAs
(e.g.,
hsa-mir-548ad-5p
hsa-mir-2113)
TFs
YAP1
TBX5)
found
significantly
correlated
conclusion,
DEGs,
relative
pathways,
genes,
miRNA
help
understanding
molecular
mechanisms
underlying
complications
progression
provide
targets
biomarkers
Abstract
Background
Sepsis
is
an
abnormal
immune
response
after
infection,
wherein
the
lung
most
susceptible
organ
to
fail,
leading
acute
injury.
To
overcome
limitations
of
current
therapeutic
strategies
and
develop
more
specific
treatment,
inflammatory
process,
in
which
T
cell-derived
extracellular
vesicles
(EVs)
play
a
central
role,
should
be
explored
deeply.
Methods
Liquid
chromatography–tandem
mass
spectrometry
was
performed
for
serum
EV
protein
profiling.
The
diacylglycerol
kinase
kappa
(DGKK)
endotoxin
contents
patients
with
sepsis-induced
injury
were
measured.
Apoptosis,
oxidative
stress,
inflammation
A549
cells,
bronchoalveolar
lavage
fluid,
tissues
mice
measured
by
flow
cytometry,
biochemical
analysis,
enzyme-linked
immunosorbent
assay,
quantitative
real-time
polymerase
chain
reaction,
western
blot.
Results
DGKK,
key
regulator
(DAG)/protein
C
(PKC)
pathway,
exhibited
elevated
expression
EVs
showed
strong
correlation
sepsis
severity
disease
progression.
DGKK
expressed
CD4
+
cells
under
regulation
NF-κB
pathway
delivered
target
including
alveolar
epithelial
cells.
produced
lymphocytes
exerted
toxic
effects
on
induce
apoptotic
cell
death,
damage,
inflammation.
In
induced
cecal
ligation
puncture,
derived
from
also
promoted
tissue
lungs.
These
attenuated
inhibition
PKC
NOX4,
downstream
effectors
DAG.
Conclusions
This
approach
established
mechanism
that
T-cell-derived
carrying
triggered
apoptosis,
inflammation,
damage
through
DAG/PKC/NOX4
pathway.
Thus,
distribution
further
investigated
Clinical Epigenetics,
Journal Year:
2025,
Volume and Issue:
17(1)
Published: Jan. 11, 2025
As
an
important
element
of
the
human
body,
iron
participates
in
numerous
physiological
and
biochemical
reactions.
In
past
decade,
ferroptosis
(a
form
iron-dependent
regulated
cell
death)
has
been
reported
to
contribute
pathogenesis
progression
various
diseases.
The
stability
cardiomyocytes
is
crucial
for
maintenance
normal
cardiac
activity.
Ferroptosis
detected
many
cardiovascular
diseases
(CVDs),
including
coronary
heart
disease,
myocardial
ischemia–reperfusion
injury,
failure,
chemotherapy-induced
damage.
cardiomyocytes,
epigenetic
regulation
post-translational
modifications
regulate
expression
ferroptosis-related
factors,
maintain
homeostasis,
participate
CVDs.
Currently,
there
no
detailed
mechanism
explain
relationship
between
this
review,
we
provide
initial
summary
core
mechanisms
with
first
focus
on
factors
context
common
We
anticipate
that
new
insights
into
CVDs
provided
here
will
inspire
development
clinical
interventions
specifically
target
active
sites
these
reducing
harmfulness
health.
Journal of Cardiothoracic Surgery,
Journal Year:
2025,
Volume and Issue:
20(1)
Published: Jan. 15, 2025
miRNA,
circRNA,
and
lncRNA
play
crucial
roles
in
the
pathogenesis
progression
of
myocardial
ischemia-reperfusion
injury
(MI/RI).
This
study
aims
to
provide
valuable
insights
into
lncRNA,
MI/RI
from
a
bibliometric
standpoint,
with
goal
fostering
further
advancements
this
area.
The
relevant
literature
field
was
retrieved
Science
Citation
Index
Expanded
(SCI-E)
database
within
Web
Science.
"Analyze
Results"
"Citation
Report"
functions
WOS
were
utilized
compile
annual
publication
citation
counts
field.
Microsoft
Office
Excel
2019
used
organize
visualize
data.
Furthermore,
visualization
analyses
countries/regions,
institutions,
authors,
keywords,
references
conducted
using
software
CiteSpace.
A
total
858
publications
included
for
analysis
published
across
297
journals,
Molecular
Medicine
Reports
contributing
highest
number
publications.
Researchers
45
countries
participated
studies
field,
those
China
most
research
hotspots
primarily
focus
on
three
areas:
role
MI/RI,
their
potential
as
therapeutic
targets,
biomarkers.
Among
these,
circular
RNA,
therapy
target,
inflammatory
response,
cardiomyocyte
ferroptosis
are
likely
emerge
emerging
trends
overall
development
is
rise.
compilation
area
may
researchers
more
assistance
selecting
directions,
ultimately
benefiting
patients.
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: Feb. 7, 2025
Ischemia-reperfusion
injury
(IRI)
is
one
of
the
leading
causes
acute
kidney
(AKI),
predisposing
patients
to
chronic
disease
(CKD)
due
maladaptive
renal
repair.
Nevertheless,
molecular
mechanisms
and
biomarkers
that
cause
repair
remain
unclear.
In
this
study,
we
used
single-nucleus
RNA
sequencing
data
from
GEO
database
(GSE139107)
identify
markers
during
transition
AKI
CKD
caused
by
IRI.
Analysis
intercellular
crosstalk,
trajectory
machine
learning
algorithms
revealed
hub
cell
clusters
genes.
Proximal
tubule
(PT)
cells,
especially
a
new
cluster
(New
PT2),
significantly
interacted
with
fibroblasts
transition.
The
expression
levels
genes
were
validated
using
bulk
RNA-seq
(GSE98622)
further
confirmed
through
RT-qPCR
immunohistochemical
analysis
in
ischemia-reperfusion
(uIRI)
mice.
Ankrd1,
gene
New
PT2,
showed
sustained
upregulation
proximal
AKI.
Compared
sham-operated
group,
Ankrd1
mice
increased
at
0.5
days
post-reperfusion,
peaked
day
1,
remained
elevated
up
60
days.
This
study
indicated
was
positively
associated
progression
may
potentially
serve
as
valuable
biomarker
for
transitional
process.
Frontiers in Cell and Developmental Biology,
Journal Year:
2024,
Volume and Issue:
12
Published: Feb. 7, 2024
Ferroptosis,
an
iron-dependent
form
of
programmed
cell
death,
introduces
a
novel
perspective
on
cellular
demise.
This
study
investigates
the
regulatory
network
exosomal
non-coding
RNAs
(ncRNAs),
including
miRNAs,
circRNAs,
and
lncRNAs,
in
ferroptosis
modulation.
The
primary
goal
is
to
examine
pathological
roles
ferroptosis-related
ncRNAs,
particularly
ischemic
reperfusion
injuries.
research
reveals
intricate
molecular
interactions
governing
interplay
between
ncRNAs
ferroptosis,
elucidating
their
diverse
different
non-malignant
contexts.
Attention
given
impact
diseases,
cardiac,
cerebral,
liver,
kidney
injuries,
as
well
lung,
wound,
neuronal
Beyond
theoretical
exploration,
provides
insights
into
potential
therapeutic
applications,
emphasizing
significance
mesenchymal
stem
cells
(MSCs)-derived
exosomes.
Findings
underscore
pivotal
role
MSC-derived
modulating
responses
related
regulation,
introducing
cutting-edge
dimension.
recognition
emphasizes
importance
exosomes
crucial
mediators
with
broad
implications.
Insights
unveil
promising
avenues
for
targeted
interventions,
capitalizing
providing
comprehensive
foundation
future
strategies.
Molecular and Cellular Biochemistry,
Journal Year:
2023,
Volume and Issue:
479(11), P. 2827 - 2841
Published: Dec. 8, 2023
Abstract
The
morbidity
and
mortality
rates
of
cardiovascular
diseases
(CVDs)
are
increasing;
thus,
they
impose
substantial
health
economic
burdens
worldwide,
effective
interventions
needed
for
immediate
resolution
this
issue.
Recent
studies
have
suggested
that
noncoding
RNAs
(ncRNAs)
play
critical
roles
in
the
occurrence
development
CVDs
potential
therapeutic
targets
novel
biomarkers
these
diseases.
Newly
discovered
modes
cell
death,
including
necroptosis,
pyroptosis,
apoptosis,
autophagy-dependent
death
ferroptosis,
also
key
CVD
progression.
However,
which
differs
from
other
aforementioned
forms
regulated
terms
morphology,
biochemistry
inhereditability,
is
a
unique
iron-dependent
mode
nonapoptotic
induced
by
abnormal
iron
metabolism
excessive
accumulation
lipid
peroxides
reactive
oxygen
species
(ROS).
Increasing
evidence
has
confirmed
ncRNA-mediated
ferroptosis
involved
regulating
tissue
homeostasis
CVD-related
pathophysiological
conditions,
such
as
cardiac
ischemia/reperfusion
(I/R)
injury,
myocardial
infarction
(MI),
atrial
fibrillation
(AF),
cardiomyopathy
heart
failure
(HF).
In
review,
we
summarize
underlying
mechanism
discuss
effects
provide
ideas
strategies.
Molecular Human Reproduction,
Journal Year:
2023,
Volume and Issue:
29(8)
Published: June 27, 2023
Abstract
The
remodeling
of
uterine
spiral
arteries
is
a
complex
process
requiring
the
dynamic
action
various
cell
types.
During
early
pregnancy,
extravillous
trophoblast
(EVT)
cells
differentiate
and
invade
vascular
wall,
replacing
smooth
muscle
(VSMCs).
Several
in
vitro
studies
have
shown
that
EVT
play
an
important
role
promoting
VSMC
apoptosis,
however,
mechanism
underlying
this
not
fully
understood.
In
study,
we
demonstrated
EVT-conditioned
media
EVT-derived
exosomes
could
induce
apoptosis.
Through
data
mining
experimental
verification,
it
was
exosome
miR-143-3p
induced
apoptosis
both
VSMCs
chorionic
plate
artery
(CPA)
model.
Furthermore,
FAS
ligand
also
expressed
on
may
co-ordinated
induction.
These
clearly
mediated
by
their
cargo
as
well
surface
presentation
FASL.
This
finding
increases
our
understanding
molecular
mechanisms
regulation
during
remodeling.