T-2
toxin,
a
natural
secondary
sesquiterpenoid
metabolite
produced
by
numerous
strains
of
Fusarium
fungi,
is
prevalent
in
both
contaminated
food
and
the
environment.
toxin
known
to
be
highly
toxic
cardiovascular
system,
but
precise
mechanisms
that
lead
toxin-induced
cardiotoxicity
are
not
yet
fully
comprehended.
Recent
findings
indicate
ferroptosis
pivotal
factor
damage
exhibits
strong
correlation
with
detrimental
impacts
toxin.
The
present
study
was
designed
examine
involvement
cardiac
injury.
Male
mice
human
cardiomyocytes
were
subjected
for
24
h
induce
acute
vivo
vitro
studies,
respectively.
Our
results
demonstrated
increased
reactive
oxygen
species
production,
malondialdehyde,
decreased
glutathione/oxidized
glutathione
adenosine
triphosphate
levels.
Furthermore,
observed
activate
ferroptosis,
as
evidenced
an
increase
iron
(Fe2+)
concentration
upregulation
prostaglandin
endoperoxide
synthase
2,
downregulation
peroxidase
4
ferritin
heavy
chain,
well
ferroptotic
morphological
alterations.
Inhibition
Liproxstatin-1
reversed
Additionally,
heme
oxgenase-1
(HO-1)
expression
exacerbates
oxidative
damage,
which
can
further
aggravated
HO-1
inhibition
Sn-protoporphyrin.
These
provide
novel
insights
into
mechanism
suggest
targeting
may
represent
promising
cardioprotective
strategy
against
Journal of Cardiovascular Development and Disease,
Journal Year:
2023,
Volume and Issue:
10(8), P. 344 - 344
Published: Aug. 12, 2023
(1)
Background:
Despite
the
evidence
that
ferroptosis
is
involved
in
myocardial
ischemia-reperfusion
(MIR),
critical
regulator
of
MIR
remains
unclear.
(2)
Methods:
We
included
three
GEO
datasets
and
a
set
ferroptosis-related
genes
with
259
genes.
Following
identification
differentially
expressed
(DEFRGs)
hub
genes,
we
performed
functional
annotation,
protein–protein
interaction
network,
immune
infiltration
analysis.
The
GSE168610
dataset,
cell
model,
an
animal
model
were
then
used
to
verify
key
(3)
Results:
identified
17
DEFRGs
9
samples
compared
control.
Heme
oxygenase
1
(Hmox1),
activating
transcription
factor
3
(Atf3),
epidermal
growth
receptor
(Egfr),
X-box
binding
protein
(Xbp1)
significantly
upregulated
response
ischemic
hypoxic
stimuli.
In
contrast,
glutathione
peroxidase
4
(Gpx4)
vascular
endothelial
A
(Vegfa)
consistently
decreased
either
oxygen
glucose
deprivation/reoxygenation
or
mouse
model.
(4)
Conclusions:
This
study
emphasized
relevance
MIR.
It
has
been
successfully
demonstrated
nine
(Hmox1,
Atf3,
Egfr,
Gpx4,
Cd44,
Vegfa,
asparagine
synthetase
(Asns),
Xbp1,
bromodomain
containing
(Brd4))
are
process.
Additional
studies
needed
explore
potential
therapeutic
targets
for
Frontiers in Cardiovascular Medicine,
Journal Year:
2023,
Volume and Issue:
10
Published: Oct. 24, 2023
Ferroptosis,
a
newly
recognized
form
of
nonapoptotic
regulated
cell
death,
is
characterized
by
iron-dependent
lipid
peroxidation.
Biological
processes,
such
as
iron
metabolism,
peroxidation,
and
amino
acid
are
involved
in
the
process
ferroptosis.
However,
related
molecular
mechanism
ferroptosis
has
not
yet
been
completely
clarified,
specific
sensitive
biomarkers
for
need
to
be
explored.
Recently,
studies
have
revealed
that
probably
causes
or
exacerbates
progress
cardiovascular
diseases,
could
potential
therapeutic
target
diseases.
In
this
review,
we
summarize
mechanisms
regulating
ferroptosis,
inducers
inhibitors
current
progresses
Furthermore,
discuss
emerging
challenges
future
perspectives,
which
may
provide
novel
insights
into
treatment
International Journal of Molecular Medicine,
Journal Year:
2024,
Volume and Issue:
54(3)
Published: July 11, 2024
It
is
considered
that
the
etiology
of
endometriosis
retrograde
menstruation
endometrial
tissue.
Although
shed
cells
are
constantly
exposed
to
a
challenging
environment
with
iron
overload,
oxidative
stress
and
hypoxia,
few
able
survive
continue
proliferate
invade.
Ferroptosis,
an
iron‑dependent
form
non‑apoptotic
cell
death,
known
play
major
role
in
development
course
endometriosis.
However,
papers
have
concentrated
on
dynamic
interaction
between
autophagy
ferroptosis
throughout
progression
diseases.
The
present
review
summarized
current
understanding
mechanisms
underlying
discuss
their
disease
progression.
For
narrative
electronic
databases
including
PubMed
Google
Scholar
were
searched
for
literature
published
up
October
31,
2023.
Autophagy
may
be
activated
at
early
stages
development.
On
other
hand,
excessive
activation
intrinsic
pathways
(e.g.,
estrogen
mechanistic
target
rapamycin)
promote
through
inhibition.
Furthermore,
suppression
cause
further
endometriotic
lesions.
In
conclusion,
dual
initiation
discussed
temporal
transition
death
regulation
during
from
endometrium
lesions
established
PLoS ONE,
Journal Year:
2024,
Volume and Issue:
19(12), P. e0314935 - e0314935
Published: Dec. 12, 2024
Disulfidptosis
is
a
newly
discovered
method
of
cell
death.
However,
no
studies
have
fully
elucidated
the
role
disulfidptosis-related
genes
(DSRGs)
in
acute
myocardial
infarction
(AMI).
The
potential
DSRGs
AMI
was
analyzed
through
comprehensive
bioinformatics
approach.
Finally,
hub
were
verified
vitro
by
qPCR.
Sixteen
DE-DSRGs
AMI.
Thereafter,
seven
determined
machine
learning
algorithms,
which
had
diagnostic
value
risk
model
showed
robust
(area
under
curve,
AUC
=
0.940).
Prognostic
analysis
revealed
prognostic
INF2
and
CD2AP.
Immune
landscape
that
closely
related
to
immune
microenvironment.
By
predictive
analysis,
we
obtained
four
miRNAs,
thirteen
small
molecule
drugs,
five
TFs
genes.
Experimental
verification
Slc3a2
Inf2
significantly
up-regulated
Dstn
down-regulated
hypoxic
model.
Our
study
demonstrated
are
disorderedly
expressed
identified
learning.
In
addition,
constructed
based
on
genes,
providing
new
perspective
for
early
diagnosis
T-2
toxin,
a
natural
secondary
sesquiterpenoid
metabolite
produced
by
numerous
strains
of
Fusarium
fungi,
is
prevalent
in
both
contaminated
food
and
the
environment.
toxin
known
to
be
highly
toxic
cardiovascular
system,
but
precise
mechanisms
that
lead
toxin-induced
cardiotoxicity
are
not
yet
fully
comprehended.
Recent
findings
indicate
ferroptosis
pivotal
factor
damage
exhibits
strong
correlation
with
detrimental
impacts
toxin.
The
present
study
was
designed
examine
involvement
cardiac
injury.
Male
mice
human
cardiomyocytes
were
subjected
for
24
h
induce
acute
vivo
vitro
studies,
respectively.
Our
results
demonstrated
increased
reactive
oxygen
species
production,
malondialdehyde,
decreased
glutathione/oxidized
glutathione
adenosine
triphosphate
levels.
Furthermore,
observed
activate
ferroptosis,
as
evidenced
an
increase
iron
(Fe2+)
concentration
upregulation
prostaglandin
endoperoxide
synthase
2,
downregulation
peroxidase
4
ferritin
heavy
chain,
well
ferroptotic
morphological
alterations.
Inhibition
Liproxstatin-1
reversed
Additionally,
heme
oxgenase-1
(HO-1)
expression
exacerbates
oxidative
damage,
which
can
further
aggravated
HO-1
inhibition
Sn-protoporphyrin.
These
provide
novel
insights
into
mechanism
suggest
targeting
may
represent
promising
cardioprotective
strategy
against
