Bioengineered,
Journal Year:
2021,
Volume and Issue:
12(1), P. 4794 - 4804
Published: Jan. 1, 2021
Dexmedetomidine
(Dex)
has
been
reported
to
exhibit
neuroprotective
effects
through
various
regulatory
mechanisms.
This
study
aims
investigate
the
role
and
molecular
mechanism
of
SNHG11
in
Dex-mediated
neuroprotection.
The
ischemic
stroke
(IS)
model
was
established
vivo
by
middle
cerebral
artery
occlusion
(MCAO)
vitro
oxygen-glucose
deprivation
reperfusion
(OGD/R)-treated
SH-SY5Y.
highly
expressed
after
OGD/R,
Dex
improved
OGD/R-induced
neurological
injury.
Additionally,
reversed
on
Furthermore,
we
found
that
upregulated
vascular
endothelial
growth
factor
A
(VEGFA)
expression
targeting
miR-324-3p.
Through
rescue
assays,
it
confirmed
regulated
injury
increasing
VEGFA
expression.
At
last,
also
discovered
improve
regulating
rat
model.
In
conclusion,
our
work
demonstrated
via
SNHG11/miR-324-3p/VEGFA
axis.
These
findings
may
offer
a
novel
therapeutic
strategy
for
IS
treatment.
Biomedicine & Pharmacotherapy,
Journal Year:
2021,
Volume and Issue:
143, P. 112132 - 112132
Published: Sept. 1, 2021
Fibrosis
is
the
endpoint
of
pathological
remodeling.
This
process
contributes
to
pathogenesis
several
chronic
disorders
and
aging-associated
organ
damage.
Different
molecular
cascades
contribute
this
process.
TGF-β,
WNT,
YAP/TAZ
signaling
pathways
have
prominent
roles
in
A
number
long
non-coding
RNAs
microRNAs
been
found
regulate
fibrosis
through
modulation
activity
related
pathways.
miR-144-3p,
miR-451,
miR-200b,
miR-328
are
among
that
participate
pathology
cardiac
fibrosis.
Meanwhile,
miR-34a,
miR-17-5p,
miR-122,
miR-146a,
miR-350
liver
different
situations.
PVT1,
MALAT1,
GAS5,
NRON,
PFL,
MIAT,
HULC,
ANRIL,
H19
We
review
impact
aging-related
pathologies.
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(10), P. 5801 - 5801
Published: May 22, 2022
In
the
last
few
years,
more
and
scientists
have
suggested
confirmed
that
epigenetic
regulators
are
tightly
connected
form
a
comprehensive
network
of
regulatory
pathways
feedback
loops.
This
is
particularly
interesting
for
better
understanding
processes
occur
in
development
progression
various
diseases.
Appearing
on
preclinical
stages
diseases,
aberrations
may
be
prominent
biomarkers.
Being
dynamic
reversible,
modifications
could
become
targets
novel
option
therapy.
Therefore,
this
review,
we
focusing
histone
ncRNAs,
their
mutual
regulation,
role
cellular
potential
clinical
application.
Biomedicine & Pharmacotherapy,
Journal Year:
2024,
Volume and Issue:
176, P. 116922 - 116922
Published: June 13, 2024
The
intricate
crosstalk
between
long
noncoding
RNAs
(lncRNAs)
and
epigenetic
modifications
such
as
chromatin/histone
methylation
acetylation
offer
new
perspectives
on
the
pathogenesis
treatment
of
kidney
diseases.
lncRNAs,
a
class
transcripts
longer
than
200
nucleotides
with
no
protein-coding
potential,
are
now
recognized
key
regulatory
molecules
influencing
gene
expression
through
diverse
mechanisms.
They
modulate
by
recruiting
or
blocking
enzymes
responsible
for
adding
removing
methyl
acetyl
groups,
DNA,
N6-methyladenosine
(m6A)
histone
acetylation,
subsequently
altering
chromatin
structure
accessibility.
In
diseases
acute
injury
(AKI),
chronic
disease
(CKD),
diabetic
nephropathy
(DN),
glomerulonephritis
(GN),
renal
cell
carcinoma
(RCC),
aberrant
patterns
DNA/RNA/histone
have
been
associated
onset
progression,
revealing
complex
interplay
lncRNA
dynamics.
Recent
studies
highlighted
how
lncRNAs
can
impact
pathology
affecting
function
genes
involved
in
cycle
control,
fibrosis,
inflammatory
responses.
This
review
will
separately
address
roles
diseases,
particular
emphasis
elucidating
bidirectional
effects
underlying
mechanisms
conjunction
addition
to
potential
exacerbating
renoprotective
pathologies.
Understanding
reciprocal
relationships
not
only
shed
light
molecular
underpinnings
pathologies
but
also
present
avenues
therapeutic
interventions
biomarker
development,
advancing
precision
medicine
nephrology.
International Journal of Molecular Sciences,
Journal Year:
2020,
Volume and Issue:
21(18), P. 6902 - 6902
Published: Sept. 20, 2020
Oxidative
stress
(OxS)
is
the
cause
and
consequence
of
metabolic
syndrome
(MetS),
incidence
economic
burden
which
increasing
each
year.
OxS
triggers
dysregulation
signaling
pathways
associated
with
metabolism
epigenetics,
including
microRNAs,
are
biomarkers
disorders.
In
this
review,
we
aimed
to
summarize
current
knowledge
regarding
interplay
between
microRNAs
in
MetS
its
components.
We
searched
PubMed
Google
Scholar
most
relevant
studies.
Collected
data
suggested
that
different
sources
(e.g.,
hyperglycemia,
insulin
resistance
(IR),
hyperlipidemia,
obesity,
proinflammatory
cytokines)
change
expression
numerous
organs
involved
regulation
glucose
lipid
endothelium.
Dysregulated
either
directly
or
indirectly
affect
and/or
activity
molecules
antioxidative
(SIRT1,
FOXOs,
Keap1/Nrf2)
along
effector
enzymes
GPx-1,
SOD1/2,
HO-1),
ROS
producers
NOX4/5),
as
well
genes
connected
inflammation,
sensitivity,
metabolism,
thus
promoting
progression
imbalance.
MicroRNAs
appear
be
important
epigenetic
modifiers
managing
delicate
redox
balance,
mediating
pro-
antioxidant
biological
impacts.
Summarizing,
may
promising
therapeutic
targets
ameliorating
repercussions
MetS.
Molecular Medicine,
Journal Year:
2021,
Volume and Issue:
27(1)
Published: July 8, 2021
Accumulating
evidences
have
demonstrated
that
long
non-coding
RNAs
(lncRNAs)
are
involved
in
the
pathophysiology
of
diabetic
nephropathy
(DN).
lncRNA
SOX2OT
plays
an
essential
role
many
diseases,
including
diabetes.
Herein,
we
aim
to
investigate
underlying
mechanism
DN
pathogenesis.
Streptozotocin-induced
mouse
models
and
high
glucose-induced
mesangial
cells
were
constructed
examine
expression
pattern
SOX2OT.
The
activation
autophagy
was
evaluated
using
immunohistochemistry,
immunofluorescence
western
blot
analysis,
respectively.
overexpressing
plasmid
applied
further
verify
functional
CCK-8
EDU
assays
performed
proliferation
cells.
Additionally,
rapamycin,
inhibitor
mTOR
signaling,
used
clarify
whether
controls
development
through
Akt/mTOR
pathway.
markedly
down-regulated
both
streptozotocin-induced
mice
Moreover,
overexpression
able
diminish
suppression
alleviate
DN-induced
renal
injury.
Functionally,
indicated
significantly
suppressed
fibrosis
obvious
inhibition
also
observed
with
overexpression,
which
then
verified
vivo.
In
summary,
alleviates
pathogenesis
via
regulating
Akt/mTOR-mediated
autophagy,
may
provide
a
novel
target
for
therapy.
Biomedicine & Pharmacotherapy,
Journal Year:
2023,
Volume and Issue:
160, P. 114340 - 114340
Published: Feb. 3, 2023
Renal
fibrosis,
an
important
pathological
change
in
the
development
of
diabetic
kidney
disease
(DKD),
urgently
needs
new
treatment
methods
clinically.
The
Jiedu
Tongluo
Baoshen
(JTBF)
formula
was
created
based
on
theory
toxic
damage
to
collaterals,
and
a
variety
active
ingredients
JTBF
have
inhibitory
effects
epithelial-mesenchymal
transition
(EMT)
extracellular
matrix
(ECM).
In
this
study,
Ultra
Performance
Liquid
Chromatography
(UPLC)
employed
analyze
effective
formula.
After
screening
PubChem
database,
we
identified
94
compounds
predicted
SIRT1
pathway
as
potential
targets
through
network
pharmacology.
addition,
high
fat
diet
(HFD)+Streptozocin
(STZ)-induced
DKD
rat
model
glucose
(HG)-induced
NRK-52E
cell
model,
activates
phosphorylation
LKB1
AMPK
enhances
autophagy
activity
cells,
thereby
reducing
accumulation
EMT
ECM.
These
results
been
confirmed
vivo
vitro
experiments.
renal
tubular
epithelial
cells
inhibits
progression
fibrosis
by
activating
SIRT1/LKB1/AMPK
signal
pathway.
This
study
provides
insights
into
molecular
mechanism
prevent
treat
fibrosis.
Journal of Diabetes Investigation,
Journal Year:
2023,
Volume and Issue:
14(9), P. 1056 - 1069
Published: June 14, 2023
Hyperglycemia
accelerates
the
development
of
diabetic
nephropathy
(DN)
by
inducing
renal
tubular
injury.
Nevertheless,
mechanism
has
not
been
elaborated
fully.
Here,
pathogenesis
DN
was
investigated
to
seek
novel
treatment
strategies.A
model
established
in
vivo,
levels
blood
glucose,
urine
albumin
creatinine
ratio
(ACR),
creatinine,
urea
nitrogen
(BUN),
malondialdehyde
(MDA),
glutathione
(GSH),
and
iron
were
measured.
The
expression
detected
qRT-PCR
Western
blotting.
H&E,
Masson,
PAS
staining
used
assess
kidney
tissue
mitochondria
morphology
observed
transmission
electron
microscopy
(TEM).
molecular
interaction
analyzed
using
a
dual
luciferase
reporter
assay.SNHG1
ACSL4
increased
tissues
mice,
but
miR-16-5p
decreased.
Ferrostatin-1
or
SNHG1
knockdown
inhibited
ferroptosis
high
glucose
(HG)-treated
HK-2
cells
db/db
mice.
Subsequently,
confirmed
be
target
for
SNHG1,
directly
targeted
ACSL4.
Overexpression
greatly
reversed
protective
roles
HG-induced
cells.SNHG1
via
miR-16-5p/ACSL4
axis
alleviate
nephropathy,
which
provided
some
new
insights
nephropathy.
Biomedicine & Pharmacotherapy,
Journal Year:
2023,
Volume and Issue:
160, P. 114361 - 114361
Published: Feb. 6, 2023
Non-coding
RNA
(ncRNA)
is
a
special
type
of
transcript
that
makes
up
more
than
90
%
the
human
genome.
Although
ncRNA
typically
does
not
encode
proteins,
it
indirectly
controls
wide
range
biological
processes,
including
cellular
metabolism,
development,
proliferation,
transcription,
and
post-transcriptional
modification.
NcRNAs
include
small
interfering
(siRNA),
PIWI-interacting
(piRNA),
tRNA-derived
(tsRNA),
etc.
The
most
researched
these
are
miRNA,
lncRNA,
circRNA,
which
crucial
regulators
in
onset
diabetes
development
associated
consequences.
ncRNAs
indicated
above
linked
to
numerous
problems
by
binding
diabetic
foot
(DF),
nephropathy,
cardiomyopathy,
peripheral
neuropathy.
According
recent
studies,
Mir-146a
can
control
AKAP12
axis
promote
proliferation
migration
ulcer
(DFU)
cells,
while
lncRNA
GAS5
activate
HIF1A/VEGF
pathway
TAF15
DFU
wound
healing.
However,
there
still
many
unanswered
questions
about
mechanism
action
ncRNAs.
In
this
study,
we
explored
new
progress
ncRNA-protein
DF,
provide
help
guidance
for
application
early
diagnosis
potential
targeted
intervention
DFU.