Flotillin- 1 ameliorates experimental diabetic retinopathy by inhibiting ferroptosis in blood-retinal barrier
Journal of Molecular Medicine,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 8, 2025
Язык: Английский
Nrf2 activation by pyrroloquinoline quinone inhibits natural aging‐related intervertebral disk degeneration in mice
Aging Cell,
Год журнала:
2024,
Номер
23(8)
Опубликована: Май 23, 2024
Abstract
Age‐related
intervertebral
disk
degeneration
(IVDD)
involves
increased
oxidative
damage,
cellular
senescence,
and
matrix
degradation.
Pyrroloquinoline
quinone
(PQQ)
is
a
water‐soluble
vitamin‐like
compound
with
strong
anti‐oxidant
capacity.
The
goal
of
this
study
was
to
determine
whether
PQQ
can
prevent
aging‐related
IVDD,
the
underlying
mechanism.
Here,
we
found
that
dietary
supplementation
for
12
months
alleviated
IVDD
phenotypes
in
aged
mice,
including
height
index
reduced
histological
scores
cell
loss,
without
toxicity.
Mechanistically,
inhibited
stress,
senescence‐associated
secretory
phenotype
(SASP)
nucleus
pulposus
annulus
fibrosus
mice.
Similarly,
protected
against
interleukin‐1β‐induced
degradation,
reactive
oxygen
species
accumulation,
senescence
human
cells
(NPCs)
vitro.
Molecular
docking
predicted
biochemical
assays
validated
interacts
specific
residues
dissociate
Keap1–Nrf2
complex,
thereby
increasing
nuclear
Nrf2
translocation
activation
Nrf2‐ARE
signaling.
RNA
sequencing
luciferase
revealed
transcriptionally
upregulate
Wnt5a
by
binding
its
promoter,
while
knockdown
prevented
inhibition
metalloproteinase‐13
NPCs.
Notably,
failed
alleviate
aging‐associated
stress
knockout
indicating
indispensable
bioactivities.
Collectively,
demonstrates
inhibits
aging‐induced
attenuating
This
clarifies
Keap1–Nrf2–Wnt5a
axis
as
novel
signaling
protective
effects
provides
evidence
potential
agent
clinical
prevention
treatment
natural
IVDD.
Язык: Английский
Cellular and Mitochondrial Pathways Contribute to SGLT2 Inhibitors-mediated Tissue Protection: Experimental and Clinical Data
Current Pharmaceutical Design,
Год журнала:
2024,
Номер
30(13), С. 969 - 974
Опубликована: Март 29, 2024
Abstract:
In
metabolic
syndrome
and
diabetes,
compromised
mitochondrial
function
emerges
as
a
critical
driver
of
cardiovascular
disease,
fueling
its
development
persistence,
culminating
in
cardiac
remodeling
adverse
events.
this
context,
angiotensin
II
-
the
main
interlocutor
renin-angiotensin-aldosterone
system
promotes
local
systemic
oxidative
inflammatory
processes.
To
highlight,
low
activity/expression
proteins
called
sirtuins
negatively
participates
these
processes,
allowing
more
significant
imbalance,
which
impacts
cellular
tissue
responses,
causing
damage,
inflammation,
vascular
remodeling.
The
reduction
energy
production
mitochondria
has
been
widely
described
element
all
types
disorders.
Additionally,
high
sirtuin
levels
AMPK
signaling
stimulate
hypoxia-inducible
factor
1
beta
promote
ketonemia.
Consequently,
enhanced
autophagy
mitophagy
advance
through
cells,
sweeping
away
debris
silencing
orchestra
stress
ultimately
protecting
vulnerable
from
damage.
highlight
particular
interest,
SGLT2
inhibitors
(SGLT2i)
profoundly
influence
mechanisms.
Randomized
clinical
trials
have
evidenced
compelling
picture
SGLT2i
emerging
game-changers,
wielding
their
power
to
demonstrably
improve
slash
rates
renal
Furthermore,
driven
by
recent
evidence,
emerge
supermolecules,
exerting
beneficial
actions
increase
efficiency,
alleviate
stress,
curb
severe
inflammation.
Its
strengthen
tissues
create
resilient
defense
against
disease.
conclusion,
like
treasure
chest
brimming
with
untold
riches,
on
holds
potential
for
health.
Unlocking
secrets,
map
guiding
adventurers
hidden
promises
pave
way
even
potent
therapeutic
strategies.
Язык: Английский
Dapagliflozin activates the RAP1B/NRF2/GPX4 signaling and promotes mitochondrial biogenesis to alleviate vascular endothelial ferroptosis
Cellular Signalling,
Год журнала:
2025,
Номер
132, С. 111824 - 111824
Опубликована: Апрель 23, 2025
Язык: Английский
Effects of Omega-3 Fatty Acids on Metabolic Syndrome and Fatty Liver Disease
Опубликована: Янв. 1, 2025
Язык: Английский
The silent saboteur: oxidative stress and the path to cognitive dysfunction
Neurodegenerative Disease Management,
Год журнала:
2025,
Номер
unknown, С. 1 - 28
Опубликована: Май 27, 2025
Oxidative
stress
(OS)
plays
a
central
role
in
age-related
cognitive
decline
and
neurodegeneration
is
increasingly
recognized
as
key
factor
the
pathogenesis
of
Alzheimer's
disease
(AD)
Parkinson's
(PD).
Elevated
OS
biomarkers
are
detectable
from
earliest
stages
these
disorders.
In
this
critical
narrative
review,
we
explore
bioenergetic
cascade
underlying
neurodegeneration,
emphasizing
pathophysiological
alterations,
mechanisms,
therapeutic
targets.
Recent
evidence
suggests
that
impaired
cellular
energy
dynamics
both
early
markers
downstream
effects
neuroinflammation,
contributing
to
symptom
severity
reduced
treatment
efficacy.
A
deeper
understanding
interrelated
processes
essential
for
development
more
effective
interventions.
Monitoring
OS-related
metabolites
may
offer
promising
strategy
identifying
targets
enabling
clinical
intervention,
ultimately
aiming
reduce
neuroinflammation
improve
patient
outcomes
AD
PD.
Язык: Английский
Adipose Tissue Macrophages-derived Exosomal MiR-500a-5p under High Glucose Promotes Adipocytes Inflammation by Suppressing Nrf2 Expression
The International Journal of Biochemistry & Cell Biology,
Год журнала:
2024,
Номер
178, С. 106713 - 106713
Опубликована: Ноя. 29, 2024
Язык: Английский
Salidroside Alleviates Myocardial Ischemia Reperfusion by Balancing Mitochondrial Homeostasis via Nrf2
Journal of Food Biochemistry,
Год журнала:
2024,
Номер
2024, С. 1 - 15
Опубликована: Фев. 14, 2024
Salidroside
(SAL),
a
phenylpropanoid
glycoside
compound
mainly
from
Rhodiola
rosea,
showed
potential
effects
on
myocardial
ischemia
reperfusion
(MIRI)
in
our
previous
studies.
The
primary
objective
of
this
investigation
was
to
study
the
mechanism
by
which
SAL
preserves
mitochondrial
homeostasis
order
provide
protection
against
MIRI.
impact
hypoxia/reoxygenation
(H/R)-induced
H9c2
cells
detected
using
CCK-8,
LDH,
and
AST.
number,
function,
morphology
mitochondria
were
examined
TEM,
RT-qPCR,
western
blot.
binding
ability
between
Nrf2
explored
through
molecular
docking
cell
thermal
shift
assay.
Combined
with
inhibitor
ML385,
results
demonstrated
that
promotes
activating
Nrf2,
decreasing
oxidative
stress,
altering
AMPK/PGC-1α/PPARα
pathway.
In
addition,
elevates
ATP
levels
improves
dynamics
imbalance
inducing
both
autophagy
mitophagy.
These
findings
highlight
therapeutic
benefits
for
cardiac
health
mitigation
Язык: Английский