Biomedicine & Pharmacotherapy,
Journal Year:
2024,
Volume and Issue:
177, P. 117093 - 117093
Published: July 5, 2024
Protein
phosphorylation
is
an
important
link
in
a
variety
of
signaling
pathways,
and
most
the
life
processes
cells
involve
protein
phosphorylation.
Based
on
amino
acid
residues
phosphorylated
proteins,
kinases
can
be
categorized
into
following
families:
serine/threonine
kinases,
tyrosine-specific
histidine-specific
tryptophan
aspartate/glutamyl
kinases.
Of
all
are
where
that
catalyze
serine
or
threonine
target
proteins
using
ATP
as
phosphate
donor.
The
current
socially
accepted
classification
to
divide
them
seven
major
groups:
kinase
A,
G,
C
(AGC),
CMGC,
Calmodulin-dependent
(CAMK),
Casein
(CK1),
STE,
Tyrosine
(TKL)
others.
After
decades
research,
preliminary
understanding
specific
respective
functions
has
entered
new
period
exploration.
In
this
paper,
we
review
literature
previous
years
introduce
pathways
related
therapeutic
modalities
played
by
each
small
family,
respectively,
some
common
cardiovascular
system
diseases
such
heart
failure,
myocardial
infarction,
ischemia-reperfusion
injury,
diabetic
cardiomyopathy.
To
certain
extent,
research
results,
including
molecular
mechanisms
methods,
fully
summarized
systematic
report
made
for
prevention
treatment
future.
Redox Biology,
Journal Year:
2023,
Volume and Issue:
67, P. 102906 - 102906
Published: Oct. 4, 2023
Microvascular
endothelial
damage
caused
by
intestinal
ischemia‒reperfusion
(II/R)
is
a
primary
catalyst
for
microcirculation
dysfunction
and
enterogenous
infection.
Previous
studies
have
mainly
focused
on
how
neutrophil
extracellular
traps
(NETs)
ferroptosis
cause
epithelial
injury,
little
attention
has
been
given
to
NETs,
from
circulatory
neutrophils,
affect
cells
during
II/R.
This
study
aimed
unravel
the
mechanisms
through
which
NETs
microvascular
dysfunction.
We
first
detected
heightened
local
NET
infiltration
around
microvasculature,
accompanied
increased
cell
ferroptosis,
resulting
in
both
human
animal
II/R
models.
However,
administration
of
inhibitor
ferrostatin-1
or
inhibition
via
neutrophil-specific
peptidylarginine
deiminase
4
(Pad4)
deficiency
led
positive
outcomes,
with
reduced
function
recovery.
Moreover,
RNA-seq
analysis
revealed
significant
enrichment
mitophagy-
ferroptosis-related
signaling
pathways
HUVECs
incubated
NETs.
Mechanistically,
elevated
formation
induced
Fundc1
phosphorylation
at
Tyr18
cells,
mitophagy
inhibition,
mitochondrial
quality
control
imbalance,
excessive
ROS
generation
lipid
peroxidation,
Nevertheless,
using
activator
urolithin
A
AAV-Fundc1
transfection
could
reverse
this
process
ameliorate
damage.
demonstrate
that
NETosis
result
microcirculatory
conclude
suppressed
can
mitigate
improving
Fundc1-dependent
mitophagy.
Targeting
be
promising
approach
treating
II/R-induced
ACS Nano,
Journal Year:
2023,
Volume and Issue:
17(13), P. 12573 - 12593
Published: June 16, 2023
Recombinant
granulocyte
colony-stimulating
factor
(G-CSF),
with
a
direct
repair
effect
on
injured
cardiomyocytes
against
myocardial
infarction
ischemia-reperfusion-injury
(IRI),
displays
poor
owing
to
the
limited
cardiac
targeting
efficacy.
There
are
almost
no
reports
of
nanomaterials
that
deliver
G-CSF
IRI
site.
Herein,
we
propose
way
protect
by
constructing
one
layer
nitric
oxide
(NO)/hydrogen
sulfide
(H2S)
nanomotors
its
outside.
NO/H2S
specific
chemotactic
ability
high
expression
reactive
oxygen
species
(ROS)/induced
synthase
(iNOS)
at
site
can
efficiently.
Meanwhile,
superoxide
dismutase
is
covalently
bound
outermost
part,
reducing
ROS
through
cascade
nanomotors.
The
synergistic
between
NO
and
H2S
effective
regulation
microenvironment
not
only
avoid
toxicity
caused
excessive
concentration
single
gas
but
also
reduce
inflammation
level
relieve
calcium
overload,
so
as
promote
play
cardioprotective
role.
Clinical and Translational Medicine,
Journal Year:
2024,
Volume and Issue:
14(7)
Published: July 1, 2024
Abstract
During
myocardial
ischaemia‒reperfusion
injury
(MIRI),
the
accumulation
of
damaged
mitochondria
could
pose
serious
threats
to
heart.
The
migrasomes,
newly
discovered
mitocytosis‐mediating
organelles,
selectively
remove
provide
mitochondrial
quality
control.
Here,
we
utilised
low‐intensity
pulsed
ultrasound
(LIPUS)
on
MIRI
mice
model
and
demonstrated
that
LIPUS
reduced
infarcted
area
improved
cardiac
dysfunction.
Additionally,
found
alleviated
MIRI‐induced
We
provided
new
evidence
mechanical
stimulation
facilitated
excretion
via
migrasome‐dependent
mitocytosis.
Inhibition
formation
migrasomes
abolished
protective
effect
MIRI.
Mechanistically,
induced
by
evoking
RhoA/Myosin
II/F‐actin
pathway.
Meanwhile,
F‐actin
activated
YAP
nuclear
translocation
transcriptionally
activate
motor
protein
KIF5B
Drp1,
which
are
indispensable
for
LIPUS‐induced
These
results
revealed
activates
mitocytosis,
a
control
mechanism,
protect
against
MIRI,
underlining
as
safe
potentially
non‐invasive
treatment
Oxidative Medicine and Cellular Longevity,
Journal Year:
2022,
Volume and Issue:
2022, P. 1 - 16
Published: Aug. 2, 2022
Mitochondria
ensure
the
supply
of
cellular
energy
through
production
ATP
via
oxidative
phosphorylation.
The
alteration
this
process,
called
mitochondrial
dysfunction,
leads
to
a
reduction
in
and
an
increase
reactive
oxygen
species
(ROS).
Mitochondrial
dysfunction
can
be
caused
by
mitochondrial/nuclear
DNA
mutations,
or
it
secondary
pathological
conditions
such
as
cardiovascular
disease,
aging,
environmental
stress.
use
therapies
aimed
at
prevention/correction
context
specific
treatment
diseases,
is
topic
growing
interest.
In
context,
data
are
conflicting
since
preclinical
studies
numerous,
but
there
no
large
randomized
studies.
Cancer Cell International,
Journal Year:
2023,
Volume and Issue:
23(1)
Published: March 10, 2023
Abstract
In
addition
to
their
lipid-lowering
functions,
statins
elicit
additional
pleiotropic
effects
on
apoptosis,
angiogenesis,
inflammation,
senescence,
and
oxidative
stress.
Many
of
these
have
been
reported
in
cancerous
noncancerous
cells
like
endothelial
(ECs),
progenitor
(EPCs)
human
umbilical
vein
(HUVCs).
Not
surprisingly,
statins'
appear
vary
largely
depending
the
cell
context,
especially
as
pertains
modulation
cycle,
apoptotic
processes.
Perhaps
most
critical
reason
for
this
discordance
is
bias
selecting
applied
doses
various
cells.
While
lower
(nanomolar)
concentrations
impose
anti-senescence,
antiapoptotic
effects,
higher
(micromolar)
precipitate
opposite
effects.
Indeed,
studies
performed
cancer
utilized
high
concentrations,
where
statin-induced
cytotoxic
cytostatic
were
noted.
Some
report
that
even
at
low
induce
senescence
or
impacts
but
not
However,
literature
appears
be
relatively
consistent
cells,
statins,
both
apoptosis
cycle
arrest,
anti-proliferative
cause
senescence.
statins’
ECs
depend
concentrations;
micromolar
while
nonomolar
act
reversely.
Heliyon,
Journal Year:
2024,
Volume and Issue:
10(7), P. e28837 - e28837
Published: April 1, 2024
Dyslipidemia
poses
a
significant
risk
to
cardiovascular
health
in
both
diabetic
and
non-diabetic
individuals.
Therefore,
it
is
crucial
normalize
lipid
homeostasis
order
prevent
or
minimize
complications
associated
with
dyslipidemia.
However,
pharmacological
interventions
for
controlling
metabolism
often
come
adverse
effects.
As
an
alternative,
utilizing
herbal-based
agents,
which
typically
have
fewer
side
effects,
holds
promise.
Crocin,
naturally
occurring
nutraceutical,
has
been
shown
impact
various
intracellular
pathways,
reduce
oxidative
stress,
alleviate
inflammatory
processes.
Recent
evidence
suggests
that
crocin
may
also
confer
lipid-related
benefits
potentially
contribute
the
normalization
of
homeostasis.
specific
advantages
cellular
pathways
involved
are
not
yet
well
understood.
In
this
review,
we
present
latest
findings
regarding
crocin,
could
be
instrumental
preventing
reducing
disorders
Additionally,
explore
potential
mechanisms
mediate
these
benefits.
Medicinal Research Reviews,
Journal Year:
2024,
Volume and Issue:
44(6), P. 2793 - 2824
Published: July 19, 2024
Nanoparticles
(NPs)
that
target
multiple
transport
mechanisms
facilitate
targeted
delivery
of
active
therapeutic
agents
to
the
central
nervous
system
(CNS)
and
improve
efficacy
across
blood-brain
barrier
(BBB).
CNS
nanotherapeutics
mostly
neurons
endothelial
cells,
however,
microglial
immune
cells
are
first
line
defense
against
neuronal
damage
brain
infections.
Through
triggering
release
inflammatory
cytokines,
chemokines
proteases,
microglia
can
however
precipitate
neurological
damage-a
significant
factor
in
neurodegenerative
diseases.
Thus,
inhibitory
attracting
much
attention
among
those
researching
developing
novel
treatments
for
disorders.
The
most
established
inhibitors
investigated
date
resveratrol,
curcumin,
quercetin,
minocycline.
there
is
great
interest
bypass
or
easily
cross
BBB.
One
such
approach
use
modified-nanocarriers
as,
for,
of,
wider
CNS.
For
inhibition,
polymeric
NPs
preferred
vehicles
choice.
Here,
we
summarize
immunologic
neuroinflammatory
role
microglia,
inhibitor
agents,
challenges
drug
delivery,
explored
inhibition
date.
We
also
discuss
applications
currently
considered
"most
useful"
microglial-inhibitor
CNS-related
