Basic Research in Cardiology,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 2, 2024
Abstract
Breast
cancer,
the
most
prevalent
cancer
affecting
women
worldwide,
poses
a
significant
cardio-oncological
burden.
Despite
advancements
in
novel
therapeutic
strategies,
anthracyclines,
HER2
antagonists,
and
radiation
remain
cornerstones
of
oncological
treatment.
However,
each
carries
risk
cardiotoxicity,
though
molecular
mechanisms
underlying
these
adverse
effects
differ.
Common
include
DNA
damage
response,
increased
reactive
oxygen
species,
mitochondrial
dysfunction,
which
are
key
areas
ongoing
research
for
potential
cardioprotective
strategies.
Since
also
essential
effective
tumor
cytotoxicity,
we
explore
tumor-specific
effects,
particularly
hereditary
breast
linked
to
BRCA1
BRCA2
mutations.
These
genetic
variants
impair
repair
mechanisms,
increase
tumorigenesis
possibly
cardiotoxicity
from
treatments
such
as
anthracyclines
antagonists.
Novel
therapies,
including
immune
checkpoint
inhibitors,
used
clinic
triple-negative
improve
outcomes
patients.
This
review
discusses
BRCA
dysfunction
associated
pathological
pathways.
It
gives
an
overview
preclinical
models
genetically
engineered
mouse
models,
syngeneic
murine
humanized
various
vitro
ex
vivo
systems
study
cardiovascular
side
therapies.
Understanding
mechanism
developing
strategies
improving
treatment
reducing
long-term
risks
ACS Nano,
Journal Year:
2024,
Volume and Issue:
18(11), P. 7890 - 7906
Published: March 6, 2024
Ferroptosis
is
a
vital
driver
of
pathophysiological
consequences
Alzheimer's
disease
(AD).
High-efficiency
pharmacological
inhibition
ferroptosis
requires
comprehensive
coordination
diverse
abnormal
intracellular
events,
which
an
urgent
problem
and
great
challenge
for
its
application
in
AD
treatment.
Herein,
triphenylphosphonium-modified
quercetin-derived
smart
nanomedicine
(TQCN)
developed
multipronged
anti-ferroptosis
therapy
AD.
Taking
advantage
the
favorable
brain-targeting
mitochondria-locating
properties,
TQCN
can
efficiently
chelate
iron
through
phytopolyphenol-mediated
spontaneous
self-assemble
into
metal-phenolic
nanocomplexes
situ,
exerting
escalating
exogenous
offensive
effects
to
attenuate
overload
induced
free
radical
burst.
Meanwhile,
Nrf2
signaling-mediated
endogenous
defensive
system
reconstituted
restore
metabolism
homeostasis
represented
by
export
storage
enhance
cytoprotective
antioxidant
cascades
lipid
peroxidation
detoxification.
Benefiting
from
multifaceted
regulation
pathogenic
processes
triggering
ferroptosis,
treatment
ameliorate
various
neurodegenerative
manifestations
associated
with
brain
deposition
rescue
severe
cognitive
decline
mice.
This
work
displays
promise
situ
self-assembled
phytopolyphenol-coordinated
intelligent
nanotherapeutics
as
advanced
candidates
against
ferroptosis-driven
progression.
Pharmacological Research,
Journal Year:
2024,
Volume and Issue:
200, P. 107057 - 107057
Published: Jan. 11, 2024
Mitochondria-associated
ferroptosis
exacerbates
cardiac
microvascular
dysfunction
in
diabetic
cardiomyopathy
(DCM).
Nicorandil,
an
ATP-sensitive
K+
channel
opener,
protects
against
endothelial
dysfunction,
mitochondrial
and
DCM;
however,
its
effects
on
mitophagy
remain
unexplored.
The
present
study
aimed
to
assess
the
beneficial
of
nicorandil
DCM
underlying
mechanisms.
Cardiac
perfusion
was
assessed
using
a
lectin
assay,
while
via
mt-Keima
transfection
transmission
electron
microscopy.
Ferroptosis
examined
mRNA
sequencing,
fluorescence
staining,
western
blotting.
localization
Parkin,
ACSL4,
AMPK
determined
immunofluorescence
staining.
Following
long-term
diabetes,
treatment
improved
function
remodeling
by
alleviating
injuries,
as
evidenced
structural
integrity.
mRNA-sequencing
biochemical
analyses
showed
that
occurred
Pink1/Parkin-dependent
suppressed
cells
after
diabetes.
Nicorandil
mitochondria-associated
promoting
mitophagy.
Moreover,
increased
phosphorylation
level
AMPKα1
promoted
translocation,
which
further
inhibited
translocation
ACSL4
ultimately
ferroptosis.
Importantly,
overexpression
mitochondria-localized
(mitoAα1)
shared
similar
benefits
with
mitophagy,
cardiovascular
protection
injury.
In
conclusion,
demonstrated
therapeutic
revealed
AMPK-Parkin-ACSL4
signaling
pathway
mediates
development
dysfunction.
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
Drug Design Development and Therapy,
Journal Year:
2024,
Volume and Issue:
Volume 18, P. 4089 - 4116
Published: Sept. 1, 2024
With
the
continuous
refinement
of
therapeutic
measures,
survival
rate
tumor
patients
has
been
improving
year
by
year,
while
cardiovascular
complications
related
to
cancer
therapy
have
become
increasingly
prominent.
Exploring
mechanism
and
prevention
strategy
therapy-related
toxicity
(CTR-CVT)
remains
one
research
hotspots
in
field
Cardio-Oncology
recent
years.
Cardiotoxicity
anticancer
drugs
involves
heart
failure,
myocarditis,
hypertension,
arrhythmias
vascular
toxicity,
mechanistically
endothelial
dysfunction,
ferroptosis,
mitochondrial
dysfunction
oxidative
stress.
To
address
cardiotoxicity
induced
different
drugs,
various
measures
put
place,
such
as
reducing
accumulation
shifting
with
less
cardiotoxicity,
using
cardioprotective
early
detection.
Due
very
limited
treatments
available
ameliorate
drugs-induced
a
few
innovations
are
being
shifted
from
animal
studies
human
studies.
Examples
include
transplantation.
Mitochondrial
transplantation
proven
be
effective
vivo
vitro
experiments.
Several
demonstrated
that
intercellular
transfer
can
doxorubicin(DOX)-induced
laying
foundation
for
innovative
therapies
cardiotoxicity.
In
this
review,
we
will
discuss
current
status
terms
pathogenesis
treatment,
focus
on
transplantation,
hope
review
bring
some
inspiration
you.
Heliyon,
Journal Year:
2024,
Volume and Issue:
10(15), P. e35219 - e35219
Published: July 28, 2024
Diabetic
cardiomyopathy
(DCM)
is
a
common
complication
of
diabetes,
and
its
pathogenesis
remains
elusive.
Ferroptosis,
process
dependent
on
iron-mediated
cell
death,
plays
crucial
role
in
DCM
via
disrupted
iron
metabolism,
lipid
peroxidation,
weakened
antioxidant
defenses.
Hyperglycemia,
oxidative
stress,
inflammation
may
exacerbate
ferroptosis
diabetes.
This
review
emphasizes
the
interaction
between
cardiac
fibroblasts
cardiomyocytes
DCM,
influencing
occurrence.
By
exploring
modulation
for
potential
therapeutic
targets,
this
article
offers
fresh
perspective
treatment.
The
study
systematically
covers
interplay,
mechanisms,
targeted
drugs
linked
to
development.
Science Advances,
Journal Year:
2024,
Volume and Issue:
10(33)
Published: Aug. 16, 2024
Ferroptosis,
caused
by
disorders
of
iron
metabolism,
plays
a
critical
role
in
various
diseases,
making
the
regulation
metabolism
essential
for
tissue
repair.
In
our
analysis
degenerated
intervertebral
disc
tissue,
we
observe
positive
correlation
between
concentration
extracellular
ions
(ex-iron)
and
severity
ferroptosis
degeneration
(IVDD).
Hence,
inspired
magnets
attracting
metals,
combine
polyether
F127
diacrylate
(FDA)
with
tannin
(TA)
to
construct
magnetically
hydrogel
(FDA-TA).
This
demonstrates
capability
adsorb
ex-iron
remodel
cells.
Furthermore,
it
exhibits
good
toughness
self-healing
properties.
Notably,
can
activate
PI3K-AKT
pathway
inhibit
nuclear
receptor
coactivator
4–mediated
ferritinophagy
under
enrichment
conditions.
The
curative
effect
related
mechanism
are
further
confirmed
vivo.
Consequently,
on
basis
pathological
mechanism,
targeted
is
designed
reshape
offering
insights
Frontiers in Medicine,
Journal Year:
2025,
Volume and Issue:
12
Published: Feb. 3, 2025
Sarcopenia
is
an
age-related
condition
characterized
by
the
progressive
loss
of
skeletal
muscle
mass
and
strength.
With
global
aging
population,
its
incidence
rapidly
increasing.
Lipid
peroxidation
a
critical
biochemical
process
that
generates
reactive
oxygen
species
(ROS),
leading
to
destruction
cell
structure
function.
It
plays
pivotal
role
in
onset
progression
sarcopenia.
This
review
summarizes
mechanisms
which
lipid
contributes
sarcopenia,
with
focus
on
regulatory
effects
membrane
damage,
mitochondrial
dysfunction,
death.
In
addition,
we
discuss
protective
antioxidant
factors
such
as
GPX4
(glutathione
peroxidase
4)
peptides
like
SS
mitigating
delaying
Finally,
potential
various
strategies,
including
natural
compounds,
supplements,
extracts,
lifestyle
interventions,
inhibiting
promoting
health
explored.
