Aging and Disease,
Journal Year:
2024,
Volume and Issue:
unknown, P. 0 - 0
Published: Jan. 1, 2024
Aging
is
a
major
risk
factor
for
cardiovascular
diseases
(CVD),
and
mitochondrial
autophagy
impairment
considered
significant
physiological
change
associated
with
aging.
Endothelial
cells
play
crucial
role
in
maintaining
vascular
homeostasis
function,
participating
various
processes
such
as
regulating
tone,
coagulation,
angiogenesis,
inflammatory
responses.
As
aging
progresses,
endothelial
worsens,
leading
to
the
development
of
numerous
diseases.
Therefore,
vital
preventing
treating
age-related
However,
there
currently
lack
systematic
reviews
this
area.
To
address
gap,
we
have
written
review
provide
new
research
therapeutic
strategies
managing
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
15
Published: March 6, 2024
Affected
by
aging,
the
elderly
diabetes
patients
have
many
pathological
characteristics
different
from
young
people,
including
more
complications,
vascular
cognitive
impairment,
osteoporosis,
and
sarcopenia.
This
article
will
explore
their
pathogenesis
mechanism
of
Traditional
Chinese
medicine
(TCM)
intervention,
use
method
systematic
review
to
evaluate
clinical
application
TCM
in
diabetes.
Cardiovascular Diabetology,
Journal Year:
2025,
Volume and Issue:
24(1)
Published: April 24, 2025
Vasculopathy
is
the
most
prevalent
complication
of
diabetes.
Endothelial
damage,
a
primary
contributor
to
hyperglycemic
vascular
complications,
impacts
macro-
and
micro-vasculatures,
causing
functional
impairment
multiple
organs.
SETD7
was
initially
identified
as
transcriptional
activator
based
on
its
ability
methylate
histone
3
lysine
4.
However,
function
in
context
diabetic
endothelial
dysfunction
remains
poorly
understood.
This
study
aims
elucidate
involvement
underlying
mechanisms
dysfunction.
knockout
mice
were
generated
investigate
effects
Streptozotocin
(STZ)-induced
hyperglycemia
injury.
Endothelial-specific
interruption
adeno-associated
virus
(AAV)
system
utilized
injury
BKS-DB(Lepr)
KO/KO
(db/db)
mice.
In
vitro
manipulation
activation
or
knockdown
conducted
assess
regulation
lipid
peroxidation,
oxidative
stress,
cell
rat
aortic
cells
(RAECs)
under
high
glucose
conditions.
Our
revealed
that
deficiency
partially
restored
damaged
attenuated
inflammatory
response
caused
by
both
STZ-induced
db/db
Moreover,
aggravated
stress
resulted
profound
through
Glutathione
Peroxidase
4
(GPX4)-mediated
peroxidation
RAECs.
Mechanistically,
reduced
p53
mono-methylation
blocked
FBXO45
transcription,
thereby
inhibiting
protein
degradation
GPX4
subsequent
well
stress.
summary,
our
demonstrates
SETD7-p53-FBXO45-GPX4
involved
glucose-induced
exacerbated
dysfunction,
which
offering
great
significance
for
mitigating
hyperglycemia-induced
damage.
Frontiers in Pharmacology,
Journal Year:
2025,
Volume and Issue:
15
Published: Jan. 6, 2025
Vascular
calcification
(VC)
commonly
occurs
in
diabetes
and
is
associated
with
cardiovascular
disease
incidence
mortality.
Currently,
there
no
drug
treatment
for
VC.
The
Danlian-Tongmai
formula
(DLTM)
a
traditional
Chinese
medicine
(TCM)
prescription
used
diabetic
VC
(DVC),
but
its
mechanisms
of
action
remain
unclear.
This
study
aims
to
elucidate
the
effects
DLTM
on
DVC
explore
underlying
action.
Ultra-high-performance
liquid
chromatography-mass
spectrometry
(UHPLC-MS)
was
identify
metabolites
DLTM.
A
rat
model
established
using
streptozotocin
(STZ)
combined
vitamin
D3
(VitD3).
were
evaluated
through
alizarin
red
staining,
calcium
deposition,
changes
osteogenic
contractile
markers.
specific
molecular
mechanism
treating
comprehensively
analyzed
by
transcriptomics,
docking
vivo
experimental
verification.
We
identified
108
major
In
vivo,
high-dose
significantly
alleviated
rats.
Transcriptomic
analysis
showed
that
markedly
altered
transcriptomic
profile
aortas,
which
regulating
CCN3/NOTCH
signaling
pathway,
promoting
vascular
smooth
muscle
contraction,
inhibiting
inflammatory
responses.
Molecular
dynamics
simulation
demonstrated
strong
binding
interactions
between
key
molecules
within
including
NOTCH1,
DLL1,
DLL4,
hes1,
hey1.
experiments
confirmed
could
upregulate
CCN3,
inhibit
activation
NOTCH
ligands
DLL1
downstream
transcription
factors
hes1
hey1,
reduce
release
cytokines
IL6,
IL1β,
TNFα.
alleviates
axis
Our
research
provides
basis
clinical
transformation
BMC Cardiovascular Disorders,
Journal Year:
2025,
Volume and Issue:
25(1)
Published: March 13, 2025
Diabetic
angiopathy
(DA)
is
a
diabetic
vascular
complication.
Pyroptosis
an
inflammatory
death
that
plays
important
role
in
the
development
of
DA,
but
underlying
mechanisms
have
not
been
fully
elucidated.
The
GSE169332
dataset
from
Gene
Expression
Omnibus
(GEO)
was
subjected
to
single-cell
RNA
sequencing
(scRNA-seq)
analysis,
and
data
mice
were
bulk
RNA-seq.
pathway
through
which
microenvironment
participated
DA
explored
by
pseudotime
analysis
cell-cell
communication.
models
constructed
using
vitro
mouse
models.
histopathological
changes
collected
aorta
observed
hematoxylin
eosin
(H&E)
Masson
staining.
distribution
expression
phenotypic
markers
related
pyroptosis
aortic
tissues
(NLRP3,
pro-Caspase1,
GSDMD-N)
immunohistochemistry
(IHC)
or
immunofluorescence
(IF)
Following
silencing
high
glucose
(HG)-induced
Impdh1
endothelial
cells
(ECs),
detected
real-time
quantitative
reverse
transcription
PCR
(qRT-PCR),
Impdh1,
NLRP3,
GSDMD
IF
staining;
cell
migration
scratch
assay,
viability
counting
kit-8
(CCK-8)
tube
formation
assay;
levels
IL-1β
IL-18
enzyme-linked
immunosorbent
assay
(ELISA)
kits.
identified
scRNA-seq
RNA-seq
as
key
molecule
progression
associated
with
ECs.
By
constructing
it
found
can
inhibit
pyroptosis.
Silencing
HG-induced
revealed
effective
amelioration
EC
damage
potential
pyroptosis-related
gene
GEO
protects
ECs
inhibiting
inflammation.
Not
applicable.
Diabetes Obesity and Metabolism,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 25, 2025
Glycaemic
therapy
in
type
1
diabetes
(T1D)
is
focused
on
insulin,
with
the
majority
of
studies
investigating
different
insulin
preparations,
delivery
devices
and
dosing
accuracy
methods.
While
deficiency
key
mechanism
for
hyperglycaemia
T1D,
individuals
this
condition
can
also
develop
resistance
(IR),
making
optimisation
glycaemia
more
challenging.
Importantly,
IR
T1D
increases
risk
both
microvascular
macrovascular
complications;
yet,
it
rarely
targeted
routine
clinical
care.
In
narrative
review,
we
briefly
discuss
mechanistic
pathways
complications
emphasising
adverse
role
IR.
We
subsequently
cover
use
adjunctive
glycaemic
therapies
improving
metabolic
profile
focusing
that
have
possible
or
definite
cardiovascular
renal
protective
properties
2
diabetes.
These
include
metformin
agents
thiazolidinedione,
Sodium-Glucose
Cotransporter-2
inhibitor
(SGLT2i)
Glucagon-Like
Peptide-1
Receptor
Agonists
(GLP-1RA)
groups.
addition
to
reviewing
these
parameters,
address
their
potential
vascular
effects
T1D.
suggest
a
pragmatic
approach
using
based
current
knowledge
benefits
risks,
while
highlighting
gaps
areas
require
further
research.
It
hoped
review
raises
awareness
offers
healthcare
professionals
simple
guidance
such
management
high-risk