Scientific Reports,
Journal Year:
2024,
Volume and Issue:
14(1)
Published: Dec. 3, 2024
Bone
marrow
mesenchymal
stem
cells
(BMMSCs)
have
garnered
attention
as
promising
therapeutic
modalities
for
spinal
cord
injury
(SCI)
due
to
their
neuroregenerative,
anti-apoptotic,
and
functional
recovery-enhancing
properties.
The
central
role
of
microRNAs
(miRNAs)
in
mediating
the
beneficial
outcomes
resulting
from
BMMSCs
SCI
has
been
highlighted
recent
studies,
suggesting
that
targeted
modulation
specific
miRNAs
holds
potential
augmenting
recovery.
Our
previous
investigation
implicated
miR-202-3p
reparative
processes
injured
cords,
although
precise
mechanistic
underpinnings
remain
elusive.
In
vivo,
were
administered
rats,
while
vitro,
was
transfected
into
PC-12
cells.
Motor
capabilities
recovery
assessed
via
Basso-Beattie-Bresnahan
(BBB)
scores
footprinting
tests;
evaluation
neuronal
tissue
repair
conducted
using
Nissl
staining,
TUNEL
hematoxylin
eosin
(HE)
immunofluorescence;
impacts
on
cellular
autophagy,
apoptosis,
relevant
pathways
evaluated
Western
blotting,
quantitative
polymerase
chain
reaction
(qPCR),
transmission
electron
microscopy
(TEM).
Functionally,
utilized
improve
motor
rats.
Histopathologically,
they
contributed
damaged
cords
regeneration
nerve
axons.
At
molecular
level,
stimulated
autophagy
suppressed
apoptosis
by
regulating
AMPK,
MAPK,
PI3K/AKT/mTOR
pathway.
Collectively,
our
findings
demonstrate
coordinate
inhibit
mTOR
activation
PI3K/AKT
pathways,
thereby
promoting
TFEB
dephosphorylation,
modulating
ultimately
fostering
post-SCI.
Biomolecules,
Journal Year:
2024,
Volume and Issue:
14(11), P. 1354 - 1354
Published: Oct. 24, 2024
Mesenchymal
stem
cells
(MSCs)
are
capable
of
differentiating
into
various
cell
types
and
play
a
crucial
role
in
repairing
aging
tissues
diseased
organs.
Aging
manifests
as
gradual
loss
cellular,
tissue,
organ
function,
leading
to
the
progression
pathologies.
Exosomes
(Exos)
extracellular
vesicles
secreted
by
cells,
which
maintain
cellular
homeostasis,
clear
debris,
facilitate
communication
between
This
review
provides
comprehensive
summary
mechanisms
for
synthesis
sorting
MSC-Exo
miRNAs
summarizes
current
research
status
MSCs-Exos
mitigating
age-related
diseases.
It
delves
underlying
molecular
mechanisms,
encompass
antioxidative
stress,
anti-inflammatory
response,
promotion
angiogenesis.
Additionally,
this
also
discusses
potential
challenges
future
strategies
advancing
miRNA-based
therapies
treatment
Current Issues in Molecular Biology,
Journal Year:
2024,
Volume and Issue:
46(5), P. 4768 - 4786
Published: May 15, 2024
The
emergence
of
combination
antiretroviral
therapy
(cART)
has
greatly
transformed
the
life
expectancy
people
living
with
HIV
(PWH).
Today,
over
76%
individuals
have
access
to
this
life-saving
therapy.
However,
progress
come
a
new
challenge:
an
increase
in
age-related
non-AIDS
conditions
among
patients
HIV.
These
manifest
earlier
PWH
than
uninfected
individuals,
accelerating
aging
process.
Like
PWH,
population
experiences
immunosenescence
marked
by
increased
proinflammatory
environment.
This
phenomenon
is
linked
chronic
inflammation,
driven
part
cellular
structures
called
inflammasomes.
Inflammatory
signaling
pathways
activated
HIV-1
infection
play
key
role
inflammasome
formation,
suggesting
crucial
link
between
and
inflammatory
state.
review
outlines
processes
triggered
aging,
focus
on
also
explores
current
research
regarding
inflammasomes
potential
strategies
for
targeting
mitigate
inflammation.
Further
presents
unique
opportunity
develop
targeted
interventions
innovative
therapeutic
modalities
combating
aging-associated
processes.
Journal of Cardiovascular Translational Research,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 28, 2024
Bufalin,
which
is
isolated
from
toad
venom,
exerts
positive
effects
on
hearts
under
pathological
circumstance.
We
aimed
to
investigate
the
and
mechanisms
of
bufalin
myocardial
I/R
injury.
In
vivo,
ameliorated
injury,
characteristics
with
better
ejection
function,
decreased
infarct
size
less
apoptosis.
The
levels
pyroptotic
proteins
were
increased
in
I/R-treated
macrophages
inflammatory
cytokines
expressed
more
I/R-induced
mouse,
could
be
attenuated
by
bufalin.
Bufalin
also
reduced
H/R-treated
macrophage
pyroptosis
vitro.
Autophagic
flux
blockage
ROS
accumulation
impaired
macrophages.
Overexpression
p62
abrogated
anti-proptosis
anti-oxidative
apoptosis
related
changed
TUNEL-positive
ratio
was
raised
cardiomyocytes
that
received
conditioned
medium
treatment
macrophages,
while
pretreatment
reduce
These
findings
indicate
may
attenuate
injury
suppressing
via
P62
pathway.
Scientific Reports,
Journal Year:
2024,
Volume and Issue:
14(1)
Published: Dec. 3, 2024
Bone
marrow
mesenchymal
stem
cells
(BMMSCs)
have
garnered
attention
as
promising
therapeutic
modalities
for
spinal
cord
injury
(SCI)
due
to
their
neuroregenerative,
anti-apoptotic,
and
functional
recovery-enhancing
properties.
The
central
role
of
microRNAs
(miRNAs)
in
mediating
the
beneficial
outcomes
resulting
from
BMMSCs
SCI
has
been
highlighted
recent
studies,
suggesting
that
targeted
modulation
specific
miRNAs
holds
potential
augmenting
recovery.
Our
previous
investigation
implicated
miR-202-3p
reparative
processes
injured
cords,
although
precise
mechanistic
underpinnings
remain
elusive.
In
vivo,
were
administered
rats,
while
vitro,
was
transfected
into
PC-12
cells.
Motor
capabilities
recovery
assessed
via
Basso-Beattie-Bresnahan
(BBB)
scores
footprinting
tests;
evaluation
neuronal
tissue
repair
conducted
using
Nissl
staining,
TUNEL
hematoxylin
eosin
(HE)
immunofluorescence;
impacts
on
cellular
autophagy,
apoptosis,
relevant
pathways
evaluated
Western
blotting,
quantitative
polymerase
chain
reaction
(qPCR),
transmission
electron
microscopy
(TEM).
Functionally,
utilized
improve
motor
rats.
Histopathologically,
they
contributed
damaged
cords
regeneration
nerve
axons.
At
molecular
level,
stimulated
autophagy
suppressed
apoptosis
by
regulating
AMPK,
MAPK,
PI3K/AKT/mTOR
pathway.
Collectively,
our
findings
demonstrate
coordinate
inhibit
mTOR
activation
PI3K/AKT
pathways,
thereby
promoting
TFEB
dephosphorylation,
modulating
ultimately
fostering
post-SCI.