Cell Biology and Toxicology,
Год журнала:
2024,
Номер
41(1)
Опубликована: Дек. 20, 2024
The
occurrence
of
severe
myocardial
ischemia/reperfusion
(I/R)
injury
is
associated
with
the
clinical
application
reestablishment
technique
for
heart
disease,
and
understanding
its
underlying
mechanisms
currently
an
urgent
issue.
Prior
investigations
have
demonstrated
potential
enhancement
MIRI
through
EGR1
suppression,
although
precise
regulatory
pathways
require
further
elucidation.
core
focus
this
investigation
to
examine
molecular
regulates
mitophagy-mediated
cell
pyroptosis
impact
on
MIRI.
Cardiomyocyte
hypoxia/reoxygenation
(H/R)
models
mouse
I/R
were
used
investigate
involvement
in
regulating
injury.
research
outcomes
that
under
H/R
conditions,
expression
was
upregulated
inhibited
JAK2/STAT3
pathway,
leading
enhanced
mitophagy
disrupted
mitochondrial
fusion/fission
dynamics,
ultimately
resulting
pyroptosis.
Further
revealed
upregulation
mediated
by
methyltransferase
like
3
(METTL3)-mediated
m6A
modification
mRNA
depended
binding
insulin
growth
factor
2
mrna
protein
(IGF2BP2)
N6-methyladenosine
(m6A)
site
enhance
stability.
In
vivo
animal
experiments
confirmed
METTL3
IGF2BP2
suppressed
activation
janus
kinase
(JAK2)
/signal
transducer
activator
transcription
(STAT3)
thereby
inhibiting
mitophagy,
disrupting
promoting
pyroptosis,
exacerbating
Journal of Neuroinflammation,
Год журнала:
2024,
Номер
21(1)
Опубликована: Ноя. 12, 2024
Abstract
Postoperative
cognitive
dysfunction
(POCD)
is
a
frequent
neurological
complication
encountered
during
the
perioperative
period
with
unclear
mechanisms
and
no
effective
treatments.
Recent
research
into
pathogenesis
of
POCD
has
primarily
focused
on
neuroinflammation,
oxidative
stress,
changes
in
neural
synaptic
plasticity
neurotransmitter
imbalances.
Given
high-energy
metabolism
neurons
their
critical
dependency
mitochondria,
mitochondrial
directly
affects
neuronal
function.
Additionally,
as
primary
organelles
generating
reactive
oxygen
species,
mitochondria
are
closely
linked
to
pathological
processes
neuroinflammation.
Surgery
anesthesia
can
induce
dysfunction,
increase
disrupt
quality-control
via
various
pathways,
hence
serving
key
initiators
process.
We
conducted
review
role
potential
postoperative
by
consulting
relevant
literature
from
PubMed
EMBASE
databases
spanning
past
25
years.
Our
findings
indicate
that
surgery
inhibit
respiration,
thereby
reducing
ATP
production,
decreasing
membrane
potential,
promoting
fission,
inducing
calcium
buffering
abnormalities
iron
accumulation,
inhibiting
mitophagy,
increasing
stress.
Mitochondrial
damage
ultimately
lead
impaired
function,
abnormal
transmission,
synthesis
release
neurotransmitters,
even
death,
resulting
dysfunction.
Targeted
therapies
have
shown
positive
outcomes,
holding
promise
novel
treatment
for
POCD.
CNS Neuroscience & Therapeutics,
Год журнала:
2024,
Номер
30(10)
Опубликована: Сен. 30, 2024
Ferroptosis,
a
form
of
programmed
cell
death
featured
by
lipid
peroxidation,
has
been
proposed
as
potential
etiology
for
postoperative
cognitive
dysfunction
(POCD).
Myocyte-specific
enhancer
factor
2C
(MEF2C),
transcription
expressed
in
various
brain
types,
implicated
disorders.
This
study
sought
to
ascertain
whether
MEF2C
governs
capacity
affecting
ferroptosis.
Frontiers in Aging Neuroscience,
Год журнала:
2025,
Номер
16
Опубликована: Янв. 13, 2025
Traumatic
brain
injury
(TBI)
can
generally
be
divided
into
focal
damage
and
diffuse
damage,
neonate
Hypoxia-Ischemia
Brain
Damage
(nHIBD)
is
one
of
the
causes
damage.
Patients
with
nHIBD
are
at
an
increased
risk
developing
Alzheimer's
disease
(AD).
However,
shared
pathogenesis
patients
affected
both
neurological
disorders
has
not
been
fully
elucidated.
We
here
aim
to
identify
molecular
signatures
between
AD.
used
integrated
analysis
cortex
gene
expression
data,
targeting
differential
genes
related
mechanisms
neurodegeneration
cognitive
impairment
following
traumatic
injury.
The
profiles
(GSE203206)
that
Neonate
(GSE23317)
were
obtained
from
Gene
Expression
Omnibus
(GEO)
database.
After
identifying
common
differentially
expressed
(DEGs)
by
limma
package
analysis,
five
kinds
analyses
performed
on
them,
namely
Ontology
(GO)
pathway
enrichment
protein-protein
interaction
network,
DEG-transcription
factor
interactions
DEG-microRNA
interactions,
protein-drug
protein-disease
association
gene-inflammation
protein-inflammation
analysis.
In
total,
12
DEGs
identified
including
HSPB1,
VIM,
MVD,
TUBB4A,
AACS,
ANXA6,
DIRAS2,
RPH3A,
CEND1,
KALM,
THOP1,
AREL1.
also
11
hub
proteins,
three
central
regulatory
transcription
factors,
microRNAs
encoded
DEGs.
Protein-drug
showed
CYC1
UQCRFS1
associated
different
drugs.
Gene-disease
shows
Mammary
Neoplasms,
Neoplasm
Metastasis,
Schizophrenia,
Ischemia
diseases
most
relevant
proteins
we
identified.
Gene-inflammation
AREL1
inflammatory
response,
while
AKT1
MAPK14
response.
This
study
provides
new
insights
AD
nHIBD.
These
pathways
could
potentially
design
therapeutic
interventions,
reducing
likelihood
development
in
survivors
neonatal
Hypoxic-Ischemia
European journal of medical research,
Год журнала:
2025,
Номер
30(1)
Опубликована: Апрель 11, 2025
Perioperative
neurocognitive
disorder
(PND)
is
a
common
neurological
complication
after
surgery/anesthesia
in
elderly
patients
that
affect
postoperative
outcome
and
long-term
quality
of
life,
which
increases
the
cost
family
social
resources.
The
pathological
mechanism
PND
complex
not
fully
understood,
methods
prevention
treatment
are
very
limited,
so
it
particularly
important
to
analyze
PND.
Research
indicates
mitochondrial
dysfunction
pivotal
initiation
progression
PND,
although
precise
mechanisms
remain
elusive
could
involve
disrupted
mitophagy.
We
reviewed
recent
studies
on
link
between
mitophagy
highlighting
role
key
proteins
abnormal
discussing
therapeutic
strategies
aimed
at
regulation.
This
provides
insights
into
underlying
potential
targets.
