Role of Oxidative Balance Score in Staging and Mortality Risk of Cardiovascular-Kidney-Metabolic Syndrome: Insights from Traditional and Machine Learning Approaches
Redox Biology,
Год журнала:
2025,
Номер
81, С. 103588 - 103588
Опубликована: Март 7, 2025
To
evaluate
the
roles
of
oxidative
balance
score
(OBS)
in
staging
and
mortality
risk
cardiovascular-kidney-metabolic
syndrome
(CKM).
Data
this
study
were
from
National
Health
Nutrition
Examination
Survey
1999-2018.
We
performed
cross-sectional
analyses
using
multinomial
logistic
regression
to
investigate
relationship
between
OBS
CKM
staging.
Cox
proportional
hazards
models
used
assess
impact
on
outcomes
patients.
Additionally,
mediation
explore
whether
mediated
relationships
specific
predictors
(Life's
Simple
7
[LS7],
systemic
immune-inflammation
index
[SII],
frailty
score)
outcomes.
Then,
machine
learning
developed
classify
stages
3/4
predict
all-cause
mortality,
with
SHapley
Additive
exPlanations
values
interpret
contribution
components.
21,609
participants
included
(20,319
CKM,
median
[IQR]
age:
52.0
[38.0-65.0]
years,
54.3%
male,
follow-up:
9.4
[5.3-14.1]
years).
Lower
quartiles
associated
advanced
Moreover,
lower
related
increased
risk,
compared
Q4
(all-cause
mortality:
Q1:
HR
1.31,
95%
CI
1.18-1.46,
Q2:
1.27,
1.14-1.42,
Q3:
1.18,
1.06-1.32;
cardiovascular
1.44,
1.16-1.79,
1.39,
1.11-1.74,
1.26,
1.01-1.57;
non-cardiovascular
1.12-1.44,
1.23,
1.08-1.40,
1.16,
1.02-1.31),
optimal
stratification
threshold
for
was
22.
(ranging
4.25%-32.85
%)
effects
SII,
LS7,
scores
light
gradient
boosting
achieved
highest
performance
predicting
(area
under
curve:
0.905)
0.875).
Cotinine
while
magnesium,
vitamin
B6,
physical
activity
protective.
This
highlights
as
a
tool
emphasizing
stress's
role
management.
Язык: Английский
Synergistic effects of lead and copper co-exposure on promoting oxidative stress and apoptosis in the neuronal cells
Toxicology,
Год журнала:
2025,
Номер
unknown, С. 154103 - 154103
Опубликована: Фев. 1, 2025
Язык: Английский
More comprehensive relationship between eGDR and sarcopenia in China: a nationwide cohort study with national representation
Diabetology & Metabolic Syndrome,
Год журнала:
2025,
Номер
17(1)
Опубликована: Март 24, 2025
Although
studies
had
shown
that
Insulin
resistance
(IR)
was
correlated
with
the
occurrence
of
sarcopenia,
there
were
still
many
controversial
conclusions.
Therefore,
we
conducted
a
more
comprehensive
study
on
relationship
between
estimated
glucose
disposal
rate
(eGDR),
an
alternative
indicator
IR,
and
risk
muscle
mass,
strength
to
clarify
their
interactions.
The
Study
included
individuals
from
China
Health
Retirement
Longitudinal
(CHARLS)
who
complete
eGDR
data
at
baseline
did
not
develop
low
mass
strength.
divided
into
four
subgroups
based
quartile
(Q)
eGDR.
lowest
(Q1)
used
as
reference.
Logistic
regression
linear
evaluate
sarcopenia
(low
strength,
possible
sarcopenia)
related
features
(ASM/Ht2,
grip,
RMS),
respectively.
In
addition,
further
evaluated
nonlinear
using
smooth
curve
fitting
threshold
effect
analysis.
results
showed
after
adjusting
for
confounders,
negatively
associated
positively
characteristics.
men
significant
reduction
in
likelihood
compared
women.
But
levels
rise,
women
gain
ASM/Ht2.
Further
analysis
revealed
inverse
correlation
ASM/Ht2
inflection
point
15.3893.
Besides
that,
grip
(7.1862)
RMS
(11.1042)
before
point.
found
higher
lower
developing
sarcopenia.
However,
effects
need
be
considered
comprehensively.
For
it
is
recommended
maintain
below
15.3893,
7.1862,
potential
benefits
early
warning
Язык: Английский
Activation of SIK1 by phanginin A regulates skeletal muscle glucose uptake by phosphorylating HADC4/5/7 and enhancing GLUT4 expression and translocation
Natural Products and Bioprospecting,
Год журнала:
2025,
Номер
15(1)
Опубликована: Апрель 7, 2025
Abstract
Salt-inducible
kinase
1
(SIK1)
participates
in
various
physiological
processes,
yet
its
involvement
regulating
skeletal
muscle
glucose
uptake
remains
unclear.
Previously,
we
showed
that
phanginin
A,
a
natural
compound
isolated
from
Caesalpinia
sappan
Linn
,
activated
SIK1
to
suppress
gluconeogenesis
hepatocytes.
Here,
aimed
elucidate
the
effects
of
on
by
using
A.
The
C2C12
myotubes
were
incubated
with
A
and
then
uptake,
mRNA
levels,
membrane
GLUT4
content,
phosphorylation
levels
proteins
SIK1/HDACs
Akt/AS160
signaling
pathways
determined.
Phanginin
significantly
promoted
while
pan-SIK
inhibitor
or
knocking
down
expression
abolished
promotion.
Further
exploration
enhanced
increasing
histone
deacetylase
(HDAC)
4/5
MEF2a
protein
level,
blocked
these
effects.
Additionally,
induced
HDAC7
phosphorylation,
upregulated
junction
plakoglobin
(JUP)
phosphorylation.
Knocking
JUP
both
attenuated
A-induced
suggesting
activation
inactivated
increase
led
upregulation
translocation
uptake.
In
vivo
study
increased
SIK1,
HDAC4/5/7,
Akt/AS160,
gene
MEF2a,
JUP,
accompanied
elevated
glycogen
content
gastrocnemius
C57BL/6
J
mice,
indicating
utilization.
These
findings
reveal
novel
mechanism
stimulates
through
phosphorylating
HADC4/5/7
subsequent
enhancement
translocation.
Graphical
abstract
Язык: Английский
Transcriptomic analysis of muscle and adipose tissues identifies myokines and adipokines contributing to lipid deposition in Taoyuan Black pigs
Animal nutrition,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 1, 2025
Язык: Английский
Integrated Metabolomics and Lipidomics Analysis Reveals the Mechanism Behind the Action of Chiglitazar on the Protection Against Sepsis-Induced Acute Lung Injury
Metabolites,
Год журнала:
2025,
Номер
15(5), С. 290 - 290
Опубликована: Апрель 25, 2025
Background:
Sepsis-induced
acute
lung
injury
(SALI)
is
a
critical
clinical
challenge
with
high
mortality.
Metabolic
dysregulation
drives
SALI
pathogenesis,
disrupting
function
and
energy
metabolism.
Despite
proven
benefits,
metabolic
restoration
underused
in
sepsis.
This
study
explores
chiglitazar's
role
balancing
metabolism
to
protect
against
SALI.
Methods:
The
protective
effects
of
chiglitazar
CLP
rats
were
demonstrated
by
the
survival
curve,
histological
analysis,
immunohistochemical
analysis
tissue.
Metabolomic
lipidomic
analyses
tissue
samples
using
gas
chromatography-mass
spectrometry
(GC-MS)
liquid
(LC-MS)
performed
evaluate
shifts
induced
surgery
pretreatment.
mRNA
protein
levels
underlying
targets
directing
nicotinamide
adenine
dinucleotide
(NAD+)
triglyceride
synthesis
analyzed
qPCR
Western
blotting.
To
validate
mechanism
which
protected
SALI,
SIRT1
inhibitor
EX-527
was
applied
human
normal
epithelial
(BEAS-2B)
cells
another
batch
observe
its
reverse
effect
action.
Results:
Chiglitazar
pretreatment
significantly
restored
NAD+
improved
dysregulated
lipid
enhancing
triglycerides
(TGs)
suppressing
accumulated
fatty
acids
(FAs).
modulation
mediated
associated
upregulations
SIRT1/PGC-1α/PPARα/GPAT3
axis.
Co-treatment
LPS-stimulated
BEAS-2B
inhibited
on
aforementioned
signaling
pathways
worsened
injury,
respectively.
Conclusions:
alleviates
restoring
TG
synthesis,
highlighting
as
promising
therapeutic
strategy
management
Язык: Английский
The Ferroptosis–Mitochondrial Axis in Depression: Unraveling the Feedforward Loop of Oxidative Stress, Metabolic Homeostasis Dysregulation, and Neuroinflammation
Xu Liu,
Qiang Luo,
Yulong Zhao
и другие.
Antioxidants,
Год журнала:
2025,
Номер
14(5), С. 613 - 613
Опубликована: Май 20, 2025
Emerging
evidence
links
ferroptosis–mitochondrial
dysregulation
to
depression
pathogenesis
through
an
oxidative
stress–energy
deficit–neuroinflammation
cycle
driven
by
iron
overload.
This
study
demonstrates
that
accumulation
initiates
ferroptosis
via
Fenton
reaction-mediated
lipid
peroxidation,
compromising
neuronal
membrane
integrity
and
disabling
the
GPx4
antioxidant
system.
Concurrent
mitochondrial
complex
I/IV
dysfunction
impairs
ATP
synthesis,
creating
AMPK/mTOR
signaling
imbalance
calcium
dyshomeostasis
synergistically
impair
synaptic
plasticity.
Bidirectional
crosstalk
emerges:
peroxidation
derivatives
oxidize
cardiolipin,
while
ROS
overproduction
activates
ACSL4
amplify
ferroptotic
susceptibility,
forming
a
self-reinforcing
neurodegenerative
loop.
Prefrontal–hippocampal
metabolomics
reveal
paradoxical
metabolic
reprogramming
with
glycolytic
compensation
suppressing
biogenesis
(via
PGC-1α/TFAM
downregulation),
trapping
neurons
in
bioenergetic
crisis.
Clinical
data
further
show
microglial
M1
polarization
cGAS-STING
activation
sustains
neuroinflammation
IL-6/TNF-α
release.
We
propose
“ferroptosis–mitochondrial
fragmentation–metabolic
maladaptation”
triad
as
mechanistic
subtyping
criteria
for
depression.
Preclinical
validation
shows
combinatorial
therapy
(iron
chelators
+
SIRT3
agonists)
rescues
viability
restoring
energy
flux.
work
shifts
therapeutic
paradigms
from
monoaminergic
targets
toward
multimodal
strategies
addressing
homeostasis,
organelle
dynamics,
vulnerability—a
framework
significant
implications
developing
neuroprotective
antidepressants.
Язык: Английский
Age‐Related Oxidative Stress and Mitochondrial Dysfunction in Lymph Node Stromal Cells Limit the Peripheral T Cell Homeostatic Maintenance and Function
Aging Cell,
Год журнала:
2025,
Номер
unknown
Опубликована: Май 21, 2025
ABSTRACT
Lymph
nodes
(LN)
are
the
key
organs
in
charge
of
long‐term
maintenance
naïve
lymphocytes
and
their
initial,
primary
activation
upon
infection.
Accumulating
evidence
indicates
that
LN
stromal
cells
undergo
degenerative
changes
with
aging
critically
impair
function,
including
generation
protective
immune
responses.
The
nature
these
defects
remains
incompletely
understood.
We
here
demonstrate
age‐related
manifest
themselves
mitochondrial
dysfunction
oxidative
stress.
Ex
vivo,
all
three
major
cell
subsets,
fibroblastic
reticular
(FRC),
lymphatic
endothelial
(LEC),
blood
(BEC)
exhibit
elevated
reactive
oxygen
species
(ROS)
stress,
reduced
potential,
mass
aging.
Old
FRC
also
exhibited
cytoplasmic
ROS
production.
This
was
accompanied
by
ability
old
to
support
Tn
survival
vitro,
a
defect
alleviated
pretreating
stroma
general
antioxidant
N
‐acetyl
cysteine
(NAC)
as
well
ROS‐reducing
(mitoquinone)
mitophagy‐inducing
(urolithin
A)
compounds.
Mitochondrial
and,
particular,
potential
were
seen
vaccination
or
infection
vivo.
Consistent
results,
vivo
treatment
mice
NAC
restored
adult
levels
numbers
antigen‐specific
CD8
+
effector
T
production
granzyme
B
response
antigenic
challenge.
Язык: Английский
Mitochondria‐Nuclear Crosstalk: Orchestrating mtDNA Maintenance
Environmental and Molecular Mutagenesis,
Год журнала:
2025,
Номер
unknown
Опубликована: Май 26, 2025
ABSTRACT
The
mitochondria
(mt)
and
nucleus
engage
in
a
dynamic
bidirectional
communication
to
maintain
cellular
homeostasis,
regulating
energy
production,
stress
response,
cell
fate.
Anterograde
signaling
directs
mt
function,
while
retrograde
conveys
metabolic
stress‐related
changes
from
the
nucleus.
Central
this
crosstalk
is
mitochondrial
DNA
(mtDNA),
which
encodes
key
oxidative
phosphorylation
components.
MtDNA
integrity
preserved
through
quality
control
mechanisms,
including
fusion
fission
dynamics,
mitophagy,
nuclear‐encoded
repair.
Disruption
these
pathways
contributes
dysfunction,
stress,
genetic
instability—hallmarks
of
aging
diseases.
Additionally,
redox
NAD+
homeostasis
integrate
nuclear
responses,
modulating
transcriptional
programs
that
support
biogenesis
adaptation.
This
review
explores
molecular
mechanisms
coordinating
mito‐nuclear
interactions,
emphasizing
their
role
maintaining
mtDNA
equilibrium.
Understanding
processes
provides
insights
into
how
dysfunction
drives
disease,
paving
way
for
targeted
therapeutic
strategies.
Язык: Английский