Mitochondrial DNA leakage: underlying mechanisms and therapeutic implications in neurological disorders
Journal of Neuroinflammation,
Год журнала:
2025,
Номер
22(1)
Опубликована: Фев. 7, 2025
Mitochondrial
dysfunction
is
a
pivotal
instigator
of
neuroinflammation,
with
mitochondrial
DNA
(mtDNA)
leakage
as
critical
intermediary.
This
review
delineates
the
intricate
pathways
leading
to
mtDNA
release,
which
include
membrane
permeabilization,
vesicular
trafficking,
disruption
homeostatic
regulation,
and
abnormalities
in
dynamics.
The
escaped
activates
cytosolic
sensors,
especially
cyclic
gmp-amp
synthase
(cGAS)
signalling
inflammasome,
initiating
neuroinflammatory
cascades
via
pathways,
exacerbating
spectrum
neurological
pathologies.
therapeutic
promise
targeting
discussed
detail,
underscoring
necessity
for
multifaceted
strategy
that
encompasses
preservation
homeostasis,
prevention
leakage,
reestablishment
dynamics,
inhibition
activation
sensors.
Advancing
our
understanding
complex
interplay
between
neuroinflammation
imperative
developing
precision
interventions
disorders.
Язык: Английский
Effect of Multidimensional Integrated Lung Protection Measures in Elderly Patients With Fragile Lungs or Combined Lung Dysfunction by Regulating AMPK/SIRT1 Pathway
Ying-Hui Cui,
Haiyong Tao,
Shi Hu
и другие.
Journal of Cellular and Molecular Medicine,
Год журнала:
2025,
Номер
29(4)
Опубликована: Фев. 1, 2025
ABSTRACT
Fragile
lungs
or
lung
dysfunction
can
significantly
impact
a
patient's
quality
of
life.
Currently,
no
specific
treatment
exists
to
prevent
in
elderly
patients.
The
detailed
mechanism
fragile
patients
remains
elusive,
and
this
study
aimed
clarify
it.
General
data
blood
specimens
were
obtained
from
with
dysfunction.
mice
exposed
cigarette
smoke
using
smoking
apparatus
induce
model.
Blood
samples
tissues
collected
all
groups
for
further
testing.
haematoxylin–eosin
(HE)
staining,
immunofluorescence,
Western
blot,
flow
cytometry
quantitative
reverse
transcriptase
PCR
(qRT‐PCR)
used
elucidate
the
molecular
mechanisms
multidimensional
integrated
protection
measures
(MILPM)
by
targeting
AMP‐activated
protein
kinase
(AMPK)/Sirtuin
1
(SIRT1)
pathway.
results
indicated
that
upregulation
AMPK/SIRT1
signalling
pathway
accelerates
process,
whereas
downregulation
Similarly,
change
forced
vital
capacity
(FVC),
total
(TLC)
levels
is
associated
reducing
their
serve
as
preventative
method
against
development.
Upregulation
accelerate
process
Язык: Английский
Reno-protective impact of diosmin and perindopril in amikacin-induced nephrotoxicity rat model: modulation of SIRT1/p53/C-FOS, NF-κB-p65, and keap-1/Nrf2/HO-1 signaling pathways
Immunopharmacology and Immunotoxicology,
Год журнала:
2025,
Номер
unknown, С. 1 - 18
Опубликована: Фев. 27, 2025
Amikacin
(AMC),
an
aminoglycoside
antibiotic
known
for
its
rapid
and
potent
bactericidal
activity,
is
also
associated
with
nephrotoxicity.
Diosmin
perindopril
have
been
reported
to
improve
renal
function
hold
promise
as
therapeutic
agents
preventing
drug-induced
This
study
aimed
investigate
the
protective
effect
of
perindopril,
either
alone
or
in
combination,
against
damage
induced
by
AMC
toxicity
elucidate
underlying
mechanisms.
The
researchers
evaluated
impact
(50
mg/kg,
orally)
(2
intraperitoneally)
on
AMC-induced
kidney
injury
(1.2
g/kg,
rats.
Invasive
blood
pressure,
serum
parameters,
oxidative
stress
biomarkers,
inflammatory
cytokine
levels
tissue
were
assessed.
Histopathological
changes
examined
using
hematoxylin
eosin
(H&E)
staining,
electron
microscopy,
immunohistochemical
analysis.
molecular
mechanisms
combination
pretreatment
investigated
enzyme-linked
immunosorbent
assay
(ELISA)
Western
blotting
techniques.
findings
demonstrated
that
therapy
improved
attenuating
pathological
observed
H&E
staining
including
tubular
necrosis
glomerular
damage,
addition
reducing
creatinine
compared
group,
urea
nitrogen
(BUN)
uric
acid,
albumin.
Mean
arterial
markers
Kidney
Injury
Molecule-1
(KIM-1),
Cystatin-c
decreased
samples
group
group.
Furthermore,
downregulated
NF-κB-p65,
P53,
Keap-1,
C-FOS,
while
upregulating
Mammalian
sirtuin
1
(SIRT1),
inhibitor
nuclear
factor
kappa
B
(Iκβ),
erythroid
2-related
2
(Nrf2),
Heme
oxygenase-1
(HO-1)
levels.
reveal
potential
clinical
application
combining
reduce
nephrotoxicity,
which
requires
further
research
settings.
Язык: Английский
Carvedilol alleviates the detrimental effects of azathioprine on hepatic tissues in experimental rats: Focusing on redox system, inflammatory and apoptosis pathways
Human & Experimental Toxicology,
Год журнала:
2024,
Номер
43
Опубликована: Апрель 1, 2024
Purpose
Drug-induced
liver
injury
is
becoming
an
increasingly
important
topic
in
drug
research
and
clinical
practice.
Due
to
a
lack
of
experimental
animal
models,
predicting
drug-induced
humans
challenging.
Azathioprine
(AZA)
classical
immunosuppressant
with
hepatotoxic
adverse
effects.
The
present
study
aimed
address
the
hepatoprotective
effect
carvedilol
(CAR)
against
AZA-induced
hepatocellular
via
assessing
redox-sensitive
signals.
Method
To
achieve
this
purpose,
rats
were
allocated
into
four
groups:
control,
CAR
only,
AZA
plus
groups.
induction
hepatic
was
induced
by
single
intraperitoneal
injection
at
dose
50
mg/kg
on
6th
day
experiment.
Each
protocol
approved
supervised
Ethics
Committee
for
Animal
Experiments.
Results
results
revealed
that
administration
significantly
diminished
dysfunction,
as
evidenced
relief
function
biomarkers
histopathological
aberration
injection.
Besides,
restored
oxidant/antioxidant
balance
well
NRF2
expression.
In
addition,
suppressed
inflammatory
response
challenge
downregulation
TLR4,
TNF-α,
MPO,
eNOS/iNOS
levels
tissue.
Moreover,
recovered
apoptotic/anti-apoptotic
status
modulation
caspase-3/Bcl2
Conclusion
Taken
together,
protects
antioxidant,
anti-inflammatory,
anti-apoptotic
activities.
These
findings
could
be
good
candidate
protection
can
added
therapeutic
regimen
reduce
their
effect.
Язык: Английский
Emerging roles of N6-methyladenosine in arsenic-induced toxicity
Rui Li,
Cuixia Wu,
Yu‐Wan Zhao
и другие.
Heliyon,
Год журнала:
2024,
Номер
10(22), С. e40473 - e40473
Опубликована: Ноя. 1, 2024
Arsenic
can
cause
extensive
toxic
damage
after
entering
the
body
of
humans
and
animals
by
altering
a
variety
events.
As
most
common
form
methylation
modification
RNA
in
eukaryotic
cells,
N
Язык: Английский
Combined Bisoprolol and Trimetazidine ameliorate Arsenic trioxide -Induced Acute Myocardial Injury in Rats: Targeting PI3K/GSK-3β/Nrf2/HO-1 and NF-κB/iNOS Signaling Pathways, Inflammatory Mediators and Apoptosis
Immunopharmacology and Immunotoxicology,
Год журнала:
2024,
Номер
unknown, С. 1 - 22
Опубликована: Ноя. 27, 2024
Background
Arsenic-trioxide
(ATO)
is
an
effective
therapy
for
acute
promyelocytic
leukemia.
Unfortunately,
its
utility
hindered
by
the
risk
of
myocardial
injury.
Both
bisoprolol
(BIS)
and
trimetazidine
(TMZ)
have
various
pharmacological
features,
including
anti-oxidant,
anti-inflammatory,
anti-apoptotic
properties.
Язык: Английский