Exploration of Medicine,
Journal Year:
2023,
Volume and Issue:
unknown, P. 127 - 156
Published: April 17, 2023
Oxygen
free
radicals
[reactive
oxygen
species
(ROS)]
and
nitrogen
(RNS)]
are
generated
by
mitochondria
during
adenosine
triphosphate
synthesis,
catalytic
activities
of
cytochrome
P450,
nicotinamide
adenine
dinucleotide
phosphate
oxidases
(NOXs),
cyclooxygenases,
nitric
oxide
synthases
drug
catabolism,
phagocytosis,
acute
inflammation.
Under
normal
circumstances,
low
levels
ROS
RNS
provide
redox
signalings
that
control
many
essential
physiological
processes.
As
age
progresses
increase
excessively
due
to
dysfunctional
mitochondria,
dysregulated
NOX,
other
free-radical
generating
sources,
leading
oxidative
stress,
which
causes
oxidation
denaturation
key
cellular
components
including
DNA,
proteins,
lipids,
become
abnormal,
constituting
damage-associated
molecular
pattern
(DAMP),
recognized
as
‘non-self’
immune
cells,
inflammation
is
mediated
nuclear
factor
kappa
B-inflammasome,
p38-c-Jun
N-terminal
kinase
Janus
kinase-signal
transducer
activator
transcription
pathways.
DAMPs
continuously
released
from
damaged
senescent
causing
an
otherwise
normally
transient
turning
into
systemic
chronic
inflammation,
the
root
cause
aging
age-associated
diseases
(AADs).
Cells
restore
balance
activating
erythroid
2-related
2
(Nrf2)
pathway
induces
synthesis
release
antioxidation
molecules
enzymes
haem
oxygenase-1,
also
inhibits
three
inflammatory
Furthermore,
upregulation
autophagy
(AP)
can
get
rid
abnormal
molecules,
prevent
generation
DAMPs,
attenuate
Both
AP
Nrf2
decrease
with
age.
The
upregulations
Nrf2,
AP,
downregulation
controlled
sensors
energy
stress
levels,
i.e.,
monophosphate-activated
protein
kinase,
silent
information
regulator
1,
Sestrins,
well
extracellular
matrix,
while
mammalian
targets
for
rapamycin
complex
a
nutrient
sensor,
act
in
opposite
direction.
If
these
sensor
systems
becomes
dysregulated,
process
accelerates,
risk
AADs
increases.
Frontiers in Endocrinology,
Journal Year:
2025,
Volume and Issue:
16
Published: March 20, 2025
Tissue
fibrosis
represents
an
aberrant
repair
process,
occurring
because
of
prolonged
injury,
sustained
inflammatory
response,
or
metabolic
disorders.
It
is
characterized
by
excessive
accumulation
extracellular
matrix
(ECM),
resulting
in
tissue
hardening,
structural
remodeling,
and
loss
function.
This
pathological
phenomenon
a
common
feature
the
end
stage
numerous
chronic
diseases.
Despite
advent
novel
therapeutic
modalities,
including
antifibrotic
agents,
these
have
only
modest
efficacy
reversing
established
are
associated
with
adverse
effects.
In
recent
years,
growing
body
research
has
demonstrated
that
exercise
significant
benefits
potential
treatment
fibrosis.
The
anti-fibrotic
effects
mediated
multiple
mechanisms,
direct
inhibition
fibroblast
activation,
reduction
expression
pro-fibrotic
factors
such
as
transforming
growth
factor-β
(TGF-β)
slowing
collagen
deposition.
Furthermore,
been
to
assist
maintaining
dynamic
equilibrium
repair,
thereby
indirectly
reducing
damage
can
also
help
maintain
balance
improving
disorders,
exerting
anti-inflammatory
antioxidant
effects,
regulating
cellular
autophagy,
restoring
mitochondrial
function,
activating
stem
cell
activity,
apoptosis,
alleviating
tissue.
paper
presents
review
its
underlying
mechanisms
for
range
fibrosis,
cardiac,
pulmonary,
renal,
hepatic,
skeletal
muscle.
offers
valuable
reference
point
non-pharmacological
intervention
strategies
comprehensive
fibrotic
BMC Gastroenterology,
Journal Year:
2025,
Volume and Issue:
25(1)
Published: April 10, 2025
Our
research
aims
to
explore
the
effects
of
different
exercise
on
liver
function
and
bile
acid
in
patients
with
non-alcoholic
fatty
disease
(NAFLD),
identify
most
beneficial
modalities
for
NAFLD.
Participants
were
randomly
divided
into
four
groups:
control
group,
aerobic
training
resistance
combined
group.
underwent
assessments
body
shape,
blood
lipid,
glucose
levels
biochemical
parameters.
Their
measured
using
LC-MS/MS
system.
Changes
these
parameters
before
after
intervention
differences
between
groups
analyzed.
AT
group
showed
significant
improvements
Additionally,
total
acids
ursodeoxycholic
significantly
increased.
The
RT
+
also
shape
parameters,
but
not
as
pronounced
those
Aerobic
is
modality
young
NAFLD,
it
improves
while
reducing
lipid
levels.
Clinical
trial
number
NCT06338449,
registered
March
22,
2024.
Lipids in Health and Disease,
Journal Year:
2025,
Volume and Issue:
24(1)
Published: April 16, 2025
Compare
the
effects
of
high-intensity
interval
training
(HIIT)
and
moderate-intensity
continuous
(MICT)
on
metabolic
dysfunction-associated
steatotic
liver
disease
(MASLD),
focusing
mechanisms
by
which
these
two
exercise
modalities
influence
gut
microbiota
structure,
bile
acid
metabolism,
intestinal
barrier
function,
as
well
their
regulatory
roles
in
hepatic
lipid
synthesis
oxidative
dynamics.
Explore
synergistic
exercise-mediated
mitochondrial
fusion
remodeling
leptin
signaling,
elucidate
causal
relationship
between
gut-derived
factors
reprogramming,
reveal
potential
multi-scale
cross-organ
dominant
exercise,
providing
a
theoretical
basis
for
systematically
comparing
different
modalities.
Thirty-two
male
rats
were
randomly
divided
into
NFD
(n
=
8)
HFD
24)
groups
fed
normal
chow
high-fat
chow,
respectively.
After
eight
weeks,
group
was
three
groups:
(1)
MICT-8;
(2)
HIIT-8;
(3)
HFD-8.
At
end
experiment,
blood,
liver,
ileum,
skeletal
muscle
samples
collected
analysis
rats'
baseline
conditions,
pathway
microbiota,
analyses.
Both
modes
ameliorated
dysregulation
attenuated
pathological
progression,
insulin
resistance,
fat
accumulation
with
MASLD.
Furthermore,
both
interventions
counteracted
HFD-induced
dysfunction
restored
gut-liver
axis
homeostasis.
HIIT
MICT
also
upregulated
acid-related
gene
expression
modulated
butyrate-producing
bacterial
taxa,
adjusted
abundance
butyrate-generating
bacteria.
improved
metabolism
MASLD
difference
not
statistically
significant.
It
is
noteworthy
that
more
effective
improving
function
than
(P
<
0.001).
World Journal of Diabetes,
Journal Year:
2025,
Volume and Issue:
16(5)
Published: April 24, 2025
BACKGROUND
Hepatitis
B
and
C
alcoholic
liver
disease
are
the
principal
causes
of
hepatic-related
morbidity
mortality.
However,
evidence
associations
between
diabetes
without
above
risk
factors
study
endpoints
is
not
well
understood.
In
addition,
effects
associated
metabolic
dysfunction
exercise
on
hepatic
outcomes
still
clear.
AIM
To
investigate
incidence
relative
hazards
cirrhosis
liver,
hepatocellular
carcinoma
(HCC),
complications
mortality
in
patients
with
type
2
(T2D)
who
were
nonalcoholic
serologically
negative
for
hepatitis
Taiwan.
METHODS
A
total
33184
T2D
648746
nondiabetic
subjects
selected
from
Taiwan’s
adult
preventive
health
care
service
linked
to
various
National
Health
Insurance
databases,
cancer
registry,
death
registry
identify
HCC,
complications,
The
Poisson
assumption
Cox
proportional
hazard
regression
model
used
estimate
incidences
all
endpoints,
respectively.
We
also
compared
stratified
by
age,
sex,
dysfunctions,
regular
subjects.
RESULTS
Compared
subjects,
had
a
significantly
greater
(6.32
vs
17.20
per
10000
person-years)
[adjusted
ratio
(aHR)
1.45;
95%CI:
1.30-1.62].
aHRs
1.81,
1.87,
2.08,
An
older
male
obesity,
hypertension,
dyslipidemia
further
increased
risks
decreased
risk,
irrespective
status.
CONCLUSION
Patients
at
mortality,
dysfunctions
provide
additional
hazard.
Coordinated
interprofessional
high-risk
education,
an
emphasis
importance
physical
activity,
crucial
minimizing
outcomes.
Exploration of Medicine,
Journal Year:
2023,
Volume and Issue:
unknown, P. 127 - 156
Published: April 17, 2023
Oxygen
free
radicals
[reactive
oxygen
species
(ROS)]
and
nitrogen
(RNS)]
are
generated
by
mitochondria
during
adenosine
triphosphate
synthesis,
catalytic
activities
of
cytochrome
P450,
nicotinamide
adenine
dinucleotide
phosphate
oxidases
(NOXs),
cyclooxygenases,
nitric
oxide
synthases
drug
catabolism,
phagocytosis,
acute
inflammation.
Under
normal
circumstances,
low
levels
ROS
RNS
provide
redox
signalings
that
control
many
essential
physiological
processes.
As
age
progresses
increase
excessively
due
to
dysfunctional
mitochondria,
dysregulated
NOX,
other
free-radical
generating
sources,
leading
oxidative
stress,
which
causes
oxidation
denaturation
key
cellular
components
including
DNA,
proteins,
lipids,
become
abnormal,
constituting
damage-associated
molecular
pattern
(DAMP),
recognized
as
‘non-self’
immune
cells,
inflammation
is
mediated
nuclear
factor
kappa
B-inflammasome,
p38-c-Jun
N-terminal
kinase
Janus
kinase-signal
transducer
activator
transcription
pathways.
DAMPs
continuously
released
from
damaged
senescent
causing
an
otherwise
normally
transient
turning
into
systemic
chronic
inflammation,
the
root
cause
aging
age-associated
diseases
(AADs).
Cells
restore
balance
activating
erythroid
2-related
2
(Nrf2)
pathway
induces
synthesis
release
antioxidation
molecules
enzymes
haem
oxygenase-1,
also
inhibits
three
inflammatory
Furthermore,
upregulation
autophagy
(AP)
can
get
rid
abnormal
molecules,
prevent
generation
DAMPs,
attenuate
Both
AP
Nrf2
decrease
with
age.
The
upregulations
Nrf2,
AP,
downregulation
controlled
sensors
energy
stress
levels,
i.e.,
monophosphate-activated
protein
kinase,
silent
information
regulator
1,
Sestrins,
well
extracellular
matrix,
while
mammalian
targets
for
rapamycin
complex
a
nutrient
sensor,
act
in
opposite
direction.
If
these
sensor
systems
becomes
dysregulated,
process
accelerates,
risk
AADs
increases.