Iron chelators loaded on myocardiocyte mitochondria-targeted nanozyme system for treating myocardial ischemia-reperfusion injury in mouse models
Ke Zhu,
No information about this author
Kun Wang,
No information about this author
Rongting Zhang
No information about this author
et al.
Journal of Nanobiotechnology,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: Feb. 15, 2025
Ferroptosis
plays
a
critical
role
in
myocardial
ischemia-reperfusion
injury
(MIRI),
posing
significant
clinical
challenge.
Nanoenzymes
like
cerium
oxide
(CeO2)
hold
promise
for
mitigating
oxidative
damage
and
inhibiting
ferroptosis,
but
their
delivery
efficiency
biological
activity
require
optimization.
This
study
aims
to
develop
targeted
nanozyme
system
MIRI
treatment
by
integrating
CeO2
with
mesoporous
polydopamine
(mPDA)
dexrazoxane
(DXZ)
achieve
synergistic
therapeutic
effects.
A
biomineralization
technique
was
used
synthesize
nanoparticles
(2–3
nm)
within
mPDA,
forming
~
130
nm
composite
(Ce@mPDA).
Surface
modifications
cardiac
homing
peptide
(CHP)
triphenylphosphine
(TPP)
enabled
hierarchical
targeting
injured
myocardium
mitochondria.
DXZ-loaded
Ce@mPDA-C/P
(D/Ce@mPDA-C/P)
were
evaluated
vitro
mouse
model
effects
on
stress,
apoptosis,
inflammation,
function.
D/Ce@mPDA-C/P
exhibited
robust
ROS
scavenging,
sustained
DXZ
release,
efficient
mitochondrial
targeting.
The
significantly
reduced
upregulated
GPX4
expression,
inhibited
modulated
the
inflammatory
microenvironment.
Long-term
studies
demonstrated
reductions
fibrosis
improvements
function,
including
enhanced
fractional
shortening
ejection
fraction.
effectively
combines
antioxidant
properties
of
iron-chelating
DXZ,
providing
promising
strategy
MIRI.
approach
may
expand
use
advance
nanomedicine-based
interventions
repair.
Language: Английский
p16INK4a Aggravated Sepsis-associated Cardiac Injury by Inhibiting the PI3K/AKT Pathway and Inducing Redox Imbalance
Journal of Cardiovascular Translational Research,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 14, 2025
Language: Английский
MiR-222-3p loaded stem cell nanovesicles repair myocardial ischemia damage via inhibiting mitochondrial oxidative stress
Mei Liu,
No information about this author
Le Wang,
No information about this author
Zhao Liu
No information about this author
et al.
Life Sciences,
Journal Year:
2025,
Volume and Issue:
unknown, P. 123447 - 123447
Published: Feb. 1, 2025
Language: Английский
Cardioprotective potential of transcription factor PRRX1 silencing against myocardial ischemia/reperfusion injury by regulating excessive mitophagy and ferroptosis through FKBP5-p38 MAPK axis
Yongpeng Fang,
No information about this author
Xudong Niu,
No information about this author
Weifang Zhao
No information about this author
et al.
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease,
Journal Year:
2025,
Volume and Issue:
1871(5), P. 167766 - 167766
Published: March 3, 2025
Language: Английский
Danqi soft caspule alleviates myocardial ischemia-reperfusion injury induced cardiomyocyte apoptosis by attenuating mitochondrial fission
Ye Yang,
No information about this author
Cuiting Lin,
No information about this author
Yan Wang
No information about this author
et al.
Frontiers in Pharmacology,
Journal Year:
2025,
Volume and Issue:
16
Published: March 12, 2025
Background
Myocardial
ischemia-reperfusion
(I/R)
injury
which
leads
to
continuously
worsening
ventricular
remodeling
and
cardiac
dysfunction
in
the
chronic
stage,
is
a
significant
contributor
global
prevalence
of
heart
failure.
Traditional
Chinese
herbal
formulas
have
been
shown
prevent
myocardial
I/R
injury.
Method
This
study
aims
investigate
whether
Danqi
soft
caspule
(DQ),
classical
traditional
medicine
(TCM)
preparation,
exerted
protective
effects
against
explore
potential
underlying
mechanisms.
A
rat
model
cell
H
2
O
induced
oxidative
stress
were
established
assess
DQ
on
injury,
cardiomyocyte
apoptosis,
as
well
mitochondrial
structure
function.
Result
pre-treatment
reduced
both
proportion
infarct
area
ischemic
risk
decreased
apoptosis
rats.
In
cells,
was
found
reduce
lower
levels.
Furthermore,
inhibited
fission,
prevented
alterations
membrane
potential,
suppressed
Cytochrome
C
release
from
mitochondria,
thereby
preventing
apoptosis.
has
by
reducing
through
inhibition
fission.
Moreover,
could
restore
function
suppressing
phosphorylation
Ca
2+
/calmodulin-dependent
protein
kinase
II
(CaMKII)
dynamin-related
1
(Drp-1).
Conclusion
fission
associated
with
CaMKII
Drp-1.
Language: Английский
The protective role of cannabidiol in stress-induced liver injury: modulating oxidative stress and mitochondrial damage
C. F. Huang,
No information about this author
Huichao Liang,
No information about this author
Xiaohua Liang
No information about this author
et al.
Frontiers in Pharmacology,
Journal Year:
2025,
Volume and Issue:
16
Published: March 14, 2025
Stress-induced
liver
injury,
resulting
from
acute
or
chronic
stress,
is
associated
with
oxidative
stress
and
inflammation.
The
endocannabinoid
system,
particularly
cannabinoid
receptor
2
(CB2R),
plays
a
crucial
role
in
damage.
However,
there
are
currently
no
clinical
drugs
targeting
CB2R
for
diseases.
Cannabidiol
(CBD),
agonist,
possesses
anti-inflammatory
antioxidant
properties.
This
study
aims
to
investigate
the
pharmacological
effects
of
CBD
mouse
model
stress-induced
injury.
We
employed
injury
evaluate
protective
CBD.
Assessments
included
histopathological
analysis,
cytokine
detection
via
ELISA,
protein
expression
analysis
using
immunohistochemistry
Western
blot,
gene
transcription
differential
analysis.
Transmission
electron
microscopy
was
utilized
observe
mitochondrial
morphology.
Additionally,
we
examined
levels
CB2R,
SLC7A11,
α-SMA,
ACSL4
proteins
elucidate
mechanisms
underlying
CBD's
effects.
exhibited
significant
against
mice.
Decreases
function
indicators
(including
Aspartate
Aminotransferase
(AST)
Alanine
(ALT))
inflammatory
cytokines
(such
as
IL-1β
Tumor
Necrosis
Factor-alpha
(TNF-α))
were
observed.
enhanced
reduced
α-SMA
levels,
mitigating
fibrosis.
It
also
decreased
increased
SOD
GSH-Px
activities,
upregulated
SLC7A11
expression.
Furthermore,
improved
morphology,
indicating
reduction
cell
death.
activates
CB2R/α-SMA
pathway
modulate
inflammation
Through
SLC7A11/ACSL4
signaling
pathway,
alleviates
enhances
reduces
These
findings
provide
theoretical
basis
potential
application
prevention
treatment
Language: Английский
Ferulic acid protects against stress-induced myocardial injury in mice
Siyong Li,
No information about this author
Peiyi He,
No information about this author
Jiahe Liu
No information about this author
et al.
Toxicology and Applied Pharmacology,
Journal Year:
2025,
Volume and Issue:
498, P. 117309 - 117309
Published: March 20, 2025
Language: Английский
Reactive oxygen species (ROS)-responsive biomaterials for treating myocardial ischemia-reperfusion injury
Ying Zhang,
No information about this author
Mantang Jiang,
No information about this author
Tao Wang
No information about this author
et al.
Frontiers in Bioengineering and Biotechnology,
Journal Year:
2024,
Volume and Issue:
12
Published: Sept. 2, 2024
Myocardial
ischemia-reperfusion
injury
(MIRI)
is
a
critical
issue
that
arises
when
restoring
blood
flow
after
an
ischemic
event
in
the
heart.
Excessive
reactive
oxygen
species
(ROS)
production
during
this
process
exacerbates
cellular
damage
and
impairs
cardiac
function.
Recent
therapeutic
strategies
have
focused
on
leveraging
ROS
microenvironment
to
design
targeted
drug
delivery
systems.
ROS-responsive
biomaterials
emerged
as
promising
candidates,
offering
enhanced
efficacy
with
reduced
systemic
adverse
effects.
This
review
examines
mechanisms
of
overproduction
myocardial
summarizes
significant
advancements
for
MIRI
treatment.
We
discuss
various
chemical
impart
sensitivity
these
materials,
emphasizing
ROS-induced
solubility
switches
degradation
mechanisms.
Additionally,
we
highlight
platforms,
such
nanoparticles
hydrogels,
their
unique
advantages
MIRI.
Preclinical
studies
demonstrating
materials
mitigating
animal
models
are
reviewed,
alongside
action
potential
clinical
implications.
also
address
challenges
future
prospects
translating
state
art
biomaterial-based
therapeutics
into
practice
improve
management
outcomes.
will
provide
valuable
insights
researchers
clinicians
working
novel
intervention.
Language: Английский
Oxidative Stress and Inflammation in Myocardial Ischemia–Reperfusion Injury: Protective Effects of Plant‐Derived Natural Active Compounds
Journal of Applied Toxicology,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Oct. 31, 2024
ABSTRACT
Acute
myocardial
infarction
(AMI)
remains
a
leading
cause
of
death
among
patients
with
cardiovascular
diseases.
Percutaneous
coronary
intervention
(PCI)
has
been
the
preferred
clinical
treatment
for
AMI
due
to
its
safety
and
efficiency.
However,
research
indicates
that
rapid
restoration
oxygen
supply
following
PCI
can
lead
secondary
injury,
termed
ischemia–reperfusion
injury
(MIRI),
posing
grave
threat
patient
survival.
Despite
ongoing
efforts,
mechanisms
underlying
MIRI
are
not
yet
fully
elucidated.
Among
them,
oxidative
stress
inflammation
stand
out
as
critical
pathophysiological
mechanisms,
playing
significant
roles
in
MIRI.
Natural
compounds
have
shown
strong
therapeutic
potential
their
high
efficacy,
availability,
low
side
effects.
Many
current
studies
indicate
natural
mitigate
by
reducing
inflammatory
responses.
Therefore,
this
paper
reviews
during
role
intervening
these
processes,
aiming
provide
basis
reference
future
development
drugs
treating
Language: Английский
PLK2 inhibited oxidative stress and ameliorated hepatic ischemia–reperfusion injury through phosphorylating GSK3β
Wenwen Ge,
No information about this author
Zhoucheng Wang,
No information about this author
Xinyang Zhong
No information about this author
et al.
Journal of Gastroenterology and Hepatology,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Nov. 19, 2024
Abstract
Background
and
Aim
Hepatic
ischemia–reperfusion
(I/R)
injury
is
the
primary
cause
of
liver
dysfunction
failure,
commonly
occurring
in
transplantation,
hepatectomy,
hemorrhagic
shock.
Polo‐like
kinase
2
(PLK2),
a
pivotal
regulator
centriole
duplication,
plays
crucial
role
cell
proliferation
repair.
However,
function
PLK2
hepatic
I/R
remains
unclear.
Methods
The
effect
was
investigated
mouse
model
hepatocyte
hypoxia‐reoxygenation
(H/R)
model.
Liver
assessed
by
serum
transaminase
hematoxylin
eosin
staining.
Cell
apoptosis
analyzed
using
TUNEL
analysis
immunoblotting.
Inflammatory
factors
were
evaluated
reverse
transcription‐quantitative
polymerase
chain
reaction.
Mice
or
cultured
cells
during
H/R
treated
overexpressing
PLK2.
ROS
fluorescence
staining
used
to
assess
oxidative
stress
injury.
Results
upregulated
after
Overexpressed
significantly
improved
enzyme
levels
alleviated
histological
Moreover,
decreased
inhibited
expression
inflammatory
liver.
Mechanistically,
increased
phosphorylation
GSK3β
enhanced
antioxidant
HO‐1,
leading
less
production.
Inhibition
HO‐1
aggravated
generation
abolished
protective
Conclusion
Overall,
these
findings
revealed
that
reduced
damage
injury,
this
related
activity.
Language: Английский