Frontiers in Physiology,
Journal Year:
2024,
Volume and Issue:
15
Published: July 12, 2024
Perivascular
adipose
tissue
(PVAT)
regulates
vascular
function
due
to
its
capacity
synthesize
vasoactive
products
and
mechanical
properties.
PVATs
most
abundant
cells
are
adipocytes,
their
populations
maintained
by
the
maturation
of
adipocyte
progenitor
(APC),
which
may
play
a
pivotal
role
in
pathogenesis
cardiovascular
diseases.
However,
distribution
APC
within
PVAT
depots,
potential
variation
spatial
location,
influence
sex
age
on
abundance
remain
unknown.
We
hypothesize
that
is
affected
age,
subtypes
have
specific
distributions.
from
thoracic
abdominal
aorta,
mesenteric
arteries,
AT
interscapular,
gonadal,
subcutaneous
depots
13-week
30-week-old
females
males
Pdgfrα-CreERT2
x
LSL-tdTomato
mice
(n
=
28)
were
analyzed.
Abdominal
aorta
had
fewer
progenitors
than
gonadal
AT.
Aging
reduced
but
increased
numbers
PVAT.
Females
more
depots.
exhibited
unique
where
they
localized
neighboring
vasa
vasorum
arteries.
(APC1,
APC2,
APC3,
diff
APC)
identified
all
Thoracic
APC3
located
adventitia
while
parenchyma.
This
study
variability
based
depot,
sex.
The
distinctive
presence
diverse
suggest
contribute
differently
diseases-induced
remodeling.
MedComm,
Journal Year:
2025,
Volume and Issue:
6(1)
Published: Jan. 1, 2025
Abstract
Sarcopenia
is
defined
as
a
muscle‐wasting
syndrome
that
occurs
with
accelerated
aging,
while
cachexia
severe
wasting
associated
conditions
such
cancer
and
immunodeficiency
disorders,
which
cannot
be
fully
addressed
through
conventional
nutritional
supplementation.
can
considered
component
of
cachexia,
the
bidirectional
interplay
between
adipose
tissue
skeletal
muscle
potentially
serving
molecular
mechanism
for
both
conditions.
However,
underlying
mechanisms
differ.
Recognizing
distinctions
these
disorders
essential
advancing
basic
translational
research
in
this
area,
enhancing
diagnostic
accuracy
ultimately
achieving
effective
therapeutic
solutions
affected
patients.
This
review
discusses
microenvironment's
changes
contributing
to
conditions,
recent
approaches
like
lifestyle
modifications,
small
molecules,
interventions,
emerging
strategies
gene
editing,
stem
cell
therapy,
gut
microbiome
modulation.
We
also
address
challenges
opportunities
multimodal
aiming
provide
insights
into
pathogenesis
sarcopenia
aiding
innovative
strategy
development
improved
treatments.
Sports Medicine,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 10, 2025
Abstract
Background
Aging
is
associated
with
sustained
low-grade
inflammation,
which
has
been
linked
to
age-related
diseases
and
mortality.
Long-term
exercise
programs
have
shown
be
effective
for
attenuating
this
process;
however,
subsequent
detraining
might
negate
some
of
these
benefits.
Master
athletes,
as
a
model
lifelong
consistent
practice,
suggested
present
similar
inflammatory
profiles
untrained
young
adults.
Nonetheless,
it
unclear
whether
maintaining
training
habits
throughout
life
can
completely
counteract
inflammation
aging.
Objectives
We
aimed
systematically
evaluate
comparisons
baseline
in
middle-aged
older
adults,
individuals
elucidate
Methods
A
systematic
review
was
conducted
following
the
Preferred
Reporting
Items
Systematic
Reviews
Meta-Analyses
(PRISMA)
statement,
protocol
prospectively
registered
PROSPERO
(CRD42024521339).
Studies
reporting
systemic
levels
proinflammatory
anti-inflammatory
markers
athletes
controls
were
eligible
inclusion.
total
six
databases
(PubMed
[MEDLINE],
Embase,
Cochrane
Central
Register
Controlled
Trials
[CENTRAL],
Scopus,
SPORTDiscus,
Web
Science
[WoS])
searched
September
2024,
studies
independently
screened
by
two
reviewers.
Risk
bias
assessed
using
an
adapted
version
Joanna
Briggs
Institute
Critical
Appraisal
tool
cross-sectional
trials,
random-effect
meta-analyses
standardized
mean
differences
(SMDs)
between
age-matched
adults
well
subjects.
Subgroup
analyses
performed
based
on
intensity
type,
participants’
sex.
Results
17
(
n
=
649
participants)
included
both
qualitative
quantitative
synthesis.
Lifelong
appears
attenuate
increases
C-reactive
protein,
elevate
interleukin
(IL)-10
compared
(C-reactive
protein:
SMD
−
0.71,
95%
confidence
interval
0.97,
0.45,
I
2
0%,
p
0.78;
IL-10:
1.44,
0.55,
2.32,
87%,
<
0.00001).
Statistical
significance
maintained
protein
IL-10
sub-analyses.
No
difference
tumor
necrosis
factor-α
observed
(SMD
0.40,
0.15,
0.96,
72%,
0.0008).
trend
towards
decreased
IL-6
pooled
comparing
rendered
statistically
significant
However,
indicated
that
still
elevated
IL-6,
along
IL-10.
Conclusions
exhibit
more
profile
denoted
circulating
and,
potentially,
increased
healthy
peers.
insufficient
changes
factor-α,
IL-10,
BMC Public Health,
Journal Year:
2025,
Volume and Issue:
25(1)
Published: Jan. 14, 2025
As
the
global
epidemic
of
obesity
fuels
metabolic
conditions,
burden
nonalcoholic
fatty
liver
disease
(NAFLD)
will
become
enormous.
Abundant
studies
revealed
association
between
high
body
mass
index
(BMI)
and
NAFLD
but
overlooked
BMI
patterns
across
life
stages.
We
aimed
to
explore
how
trajectories
over
age
relate
NAFLD.
Selecting
3212
participants
in
NHANES
2017–2020,
we
tracked
records
at
different
ages.
Using
a
latent
class
trajectory
model
(LCTM),
identified
age.
Multinomial
logistic
regression
assessed
their
with
advanced
fibrosis.
Structural
equation
modeling
(SEM)
mediation
effects.
3
trajectories:
Steady
Progression,
Increase
Decrease,
Rapid
Ascending.
There
was
no
significant
difference
NAFLD/advanced
fibrosis
risk
increase-to-decrease
group
steady
progression
group.
The
Ascending
significantly
correlated
(OR
=
2.21,
95%
CI
1.29–3.77)
3.04,
1.13–8.22).
This
influenced
by
chain-mediated
process
phenotypic
C-reactive
protein
(mediated
effect
0.010,
p
<
0.01;
mediated
0.003,
0.05).
on
independent
insulin
resistance
(IR).
rapid
ascending
more
pronounced
among
male
subgroup
(p
for
interaction
0.008).
correlates
an
increased
susceptibility
BMI,
aging
inflammation.
Our
results
suggest
that
long-term
maintenance
is
pivotal
prevention.
Aging-inflammation
may
represent
distinct
mechanism
sustained
NAFLD,
IR.
Lipids in Health and Disease,
Journal Year:
2025,
Volume and Issue:
24(1)
Published: Jan. 24, 2025
Ageing
results
in
diminished
adaptability,
as
well
declines
physiological
and
psychological
functions
resilience.
The
epigenetic
clock
'Phenotypic
Age'
(PhenoAge)
represents
'preclinical
ageing'.
Phenotypic
Age
Acceleration
(PhenoAgeAccel)
is
defined
the
residual
from
a
linear
regression
model
predicting
PhenoAge
on
basis
of
chronological
age.
Abdominal
subcutaneous
adipose
tissue,
visceral
Homeostasis
Model
Assessment
Insulin
Resistance
(HOMA-IR),
high-density
lipoprotein
cholesterol
(HDL-C)
have
all
been
shown
to
correlate
with
ageing;
however,
connections
between
these
factors
are
still
insufficiently
investigated.
Data
for
this
study
were
sourced
National
Health
Nutrition
Examination
Survey
(2015–2018),
comprising
2580
participants.
Complex
survey
designs
considered.
To
examine
association
body
fat
area
PhenoAgeAccel,
logistic
was
applied.
Additionally,
subgroup
analysis
used
identify
variations
population
characteristics.
dose‒response
relationship
PhenoAgeAccel
determined
via
restricted
cubic
spline
analysis.
Mediation
interaction
analyses
further
employed
investigate
roles
HOMA-IR
HDL-C
association.
In
nonelderly
adults,
relationships
differed
For
abdominal
(SFA),
nonlinear
individuals
aged
18–44
years
45–59
years,
thresholds
2.969
m²
3.394
m²,
respectively.
contrast,
(VFA)
observed
while
0.769
1.220
effect
revealed
that
had
more
pronounced
mediation
accounting
13.4%
VFA
6.9%
SFA
PhenoAgeAccel.
Conversely,
greater
mediating
21.7%
11.6%
≥
2.73
or
>
0.925
3.137
accelerated
PhenoAge,
whereas
1.60
<
≤
3.90
mmol/L
combined
decelerated
PhenoAge.
study,
among
SFA,
VFA,
elucidated,
characteristic
across
different
age
groups
identified.
emphasize
complex
influence
distribution
ageing
process
refine
various
cohorts.
These
findings
provide
biological
future
screening
appropriate
intervention
high-risk
populations
offer
valuable
insights
guiding
personalized
clinical
interventions
health
management
strategies.
Nature Aging,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 5, 2025
Aging
leads
to
progressive
decline
in
organ
and
tissue
integrity
function,
partly
due
loss
of
proteostasis
autophagy
malfunctioning.
A
decrease
with
age
chaperone-mediated
(CMA),
a
selective
type
lysosomal
degradation,
has
been
reported
various
organs
cells
from
rodents
humans.
Disruption
CMA
recapitulates
features
aging,
whereas
activating
mice
protects
against
age-related
diseases
such
as
Alzheimer's,
retinal
degeneration
and/or
atherosclerosis.
However,
sex-specific
cell-type-specific
differences
aging
remain
unexplored.
Here,
using
reporter
single-cell
transcriptomic
data,
we
report
that
most
cell
types
show
age,
males
exhibiting
greater
aging.
Reduced
is
often
associated
fewer
lysosomes
competent
for
CMA.
Transcriptional
downregulation
genes
may
further
contribute
decline,
especially
males.
These
findings
suggest
influence
vulnerability
degeneration.
Using
imaging
fluorescent
(CMA)
RNA
sequencing
the
authors
present
resource
on
basal
activity
across
organs,
sexes
young
old
mice,
offering
comprehensive
overview
changes
this
proteostatic
mechanism
context