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.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(2), P. 897 - 897
Published: Jan. 11, 2024
The
hospital
mortality
in
patients
with
ST-segment
elevation
myocardial
infarction
(STEMI)
is
about
6%
and
has
not
decreased
recent
years.
leading
cause
of
death
these
ischemia/reperfusion
(I/R)
cardiac
injury.
It
quite
obvious
that
there
an
urgent
need
to
create
new
drugs
for
the
treatment
STEMI
based
on
knowledge
pathogenesis
I/R
injury,
particular,
molecular
mechanism
ferroptosis.
In
this
study,
it
was
demonstrated
ferroptosis
involved
development
antitumor
drug-induced
cardiomyopathy,
diabetic
septic
inflammation.
There
indirect
evidence
participates
stress-induced
activation
AMPK,
PKC,
ERK1/2,
PI3K,
Akt
prevents
inhibition
HO-1
alleviates
roles
GSK-3β
NOS
regulation
require
further
study.
stimulation
Nrf2,
STAT3
TLR4
NF-κB
promotes
cardiomyocytes.
MiR-450b-5p
miR-210-3p
can
increase
tolerance
cardiomyocytes
hypoxia/reoxygenation
through
Circ_0091761
RNA,
miR-214-3p,
miR-199a-5p,
miR-208a/b,
miR-375-3p,
miR-26b-5p
miR-15a-5p
aggravate
Biomedicine & Pharmacotherapy,
Journal Year:
2024,
Volume and Issue:
177, P. 117081 - 117081
Published: July 5, 2024
The
discovery
of
an
inhibitor
for
acyl-CoA
synthetase
long-chain
family
member
4
(ACSL4),
a
protein
involved
in
the
process
cell
injury
through
ferroptosis,
has
potential
to
ameliorate
damage.
In
this
study,
we
aimed
investigate
berberine
(BBR)
as
ACSL4
order
suppress
endothelial
ferroptosis
and
provide
protection
against
atherosclerosis.
An
atherosclerosis
model
was
created
ApoE
Biomedicine & Pharmacotherapy,
Journal Year:
2024,
Volume and Issue:
175, P. 116689 - 116689
Published: May 3, 2024
Ischemic
heart
disease
invariably
leads
to
devastating
damage
human
health.
Nicotinamide
ribose
(NR),
as
one
of
the
precursors
NAD+
synthesis,
has
been
discovered
exert
a
protective
role
in
various
neurological
and
cardiovascular
disorders.
Our
findings
demonstrated
that
pretreatment
with
200
mg/kg
NR
for
3
h
significantly
reduced
myocardial
infarct
area,
decreased
levels
CK-MB
LDH
serum,
improved
cardiac
function
rats
during
ischemia-reperfusion
(I/R)
injury.
Meanwhile,
0.5
mM
also
effectively
increased
viability
release
H9c2
cells
OGD/R.
We
had
provided
evidence
could
decrease
mitochondrial
reactive
oxygen
species
(mtROS)
production
MDA
content,
enhance
SOD
activity,
thereby
mitigating
inhibiting
apoptosis
I/R
Further
investigations
revealed
content
upregulated
SIRT3
protein
expression
myocardium.
Through
using
small
interfering
RNA
deacetylase
activity
inhibitor
3-TYP,
we
confirmed
cardioprotective
effect
on
cardiomyocytes
was
largely
dependent
inhibition
oxidative
stress
via
SIRT3-SOD2
axis.
Overall,
our
study
suggested
exogenous
supplementation
mitigated
inhibited
injury
by
reducing
SIRT3-SOD2-mtROS
pathway.
Redox Biology,
Journal Year:
2024,
Volume and Issue:
76, P. 103321 - 103321
Published: Aug. 19, 2024
Cell
death
constitutes
a
critical
component
of
the
pathophysiology
cardiovascular
diseases.
A
growing
array
non-apoptotic
forms
regulated
cell
(RCD)-such
as
necroptosis,
ferroptosis,
pyroptosis,
and
cuproptosis-has
been
identified
is
intimately
linked
to
various
conditions.
These
RCD
are
governed
by
genetically
programmed
mechanisms
within
cell,
with
epigenetic
modifications
being
common
crucial
regulatory
method.
Such
include
DNA
methylation,
RNA
histone
acetylation,
non-coding
RNAs.
This
review
recaps
roles
modifications,
RNAs
in
diseases,
well
which
regulate
key
proteins
involved
death.
Furthermore,
we
systematically
catalog
existing
pharmacological
agents
targeting
novel
their
action
article
aims
underscore
pivotal
role
precisely
regulating
specific
pathways
thus
offering
potential
new
therapeutic
avenues
that
may
prove
more
effective
safer
than
traditional
treatments.
