Advances in intrahepatic and extrahepatic vascular dysregulations in cirrhotic portal hypertension
Frontiers in Medicine,
Journal Year:
2025,
Volume and Issue:
12
Published: Jan. 31, 2025
Cirrhotic
portal
hypertension,
the
most
prevalent
and
clinically
significant
complication
of
liver
cirrhosis,
manifests
as
elevated
venous
pressure
is
associated
with
severe
complications.
Although
much
research
on
mechanisms
hypertension
has
focused
fibrosis,
less
attention
been
given
to
role
intrahepatic
extrahepatic
vascular
dysfunction,
particularly
respect
vasculature.
While
hepatic
fibrosis
in
cirrhotic
undeniable,
underlying
involving
vasculature
are
highly
complex.
Sinusoidal
capillarization
endothelial
dysfunction
contribute
increased
resistance.
Hemodynamic
changes
circulation,
including
splanchnic
vasodilation
hyperdynamic
play
a
development
hypertension.
Additionally,
therapeutic
strategies
targeting
these
diverse,
improvement
sinusoidal
microcirculation,
therapies
stellate
cells
activation,
pharmacological
modulation
systemic
tone.
Therefore,
this
review,
we
will
discuss
vascular-related
treatment
progress
cirrhosis
provide
new
theoretical
basis
practical
guidance
for
clinical
treatment.
Language: Английский
Protocol for monitoring intrapulmonary vasodilation in mice using contrast-enhanced echocardiography
Nityanand Bolshette,
No information about this author
Hanna Bueno-Levy,
No information about this author
Gad Asher
No information about this author
et al.
STAR Protocols,
Journal Year:
2025,
Volume and Issue:
6(1), P. 103647 - 103647
Published: Feb. 20, 2025
Language: Английский
Control of circadian muscle glucose metabolism through the BMAL1–HIF axis in obesity
Proceedings of the National Academy of Sciences,
Journal Year:
2025,
Volume and Issue:
122(13)
Published: March 24, 2025
Disruptions
of
circadian
rhythms
are
widespread
in
modern
society
and
lead
to
accelerated
worsened
symptoms
metabolic
syndrome.
In
healthy
mice,
the
clock
factor
BMAL1
is
required
for
skeletal
muscle
function
metabolism.
However,
importance
development
diseases,
such
as
diet-induced
obesity
(DIO),
remains
unclear.
Here,
we
demonstrate
that
muscle–specific
BMAL1-deficient
mice
exhibit
glucose
tolerance
upon
high-fat
diet
feeding,
despite
no
evidence
increased
weight
gain.
Metabolite
profiling
from
Bmal1
-deficient
muscles
revealed
impaired
utilization
specifically
at
early
steps
glycolysis
dictate
switch
between
anabolic
catabolic
fate.
We
provide
this
due
abnormal
control
nutrient
stress–responsive
hypoxia-inducible
(HIF)
pathway.
Genetic
HIF1α
stabilization
restores
expression
217/736
dysregulated
genes
during
DIO,
including
glycolytic
enzymes.
Together,
these
data
indicate
an
important
regulator
HIF-driven
flexibility,
which
influences
high-fat-diet-induced
intolerance.
Language: Английский
Integrating cancer medicine into metabolic rhythms
Keyu Su,
No information about this author
Deshun Zeng,
No information about this author
Weiru Zhang
No information about this author
et al.
Trends in Endocrinology and Metabolism,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 1, 2025
Language: Английский
Heart-attack outcomes are worse in the morning when activity of protein duo dips
Nature,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 23, 2025
Language: Английский
Circadian clock controlled glycolipid metabolism and its relevance to disease management
Luomin Lin,
No information about this author
Yuwei Huang,
No information about this author
Aijing Li
No information about this author
et al.
Biochemical Pharmacology,
Journal Year:
2025,
Volume and Issue:
unknown, P. 116967 - 116967
Published: April 1, 2025
Language: Английский
Disruption of Hepatic Sinusoidal Homeostasis Leads to Hepatopulmonary Syndrome
Jiaxin Chen,
No information about this author
Yangkun Guo,
No information about this author
Xiaoxun Zhang
No information about this author
et al.
Journal of Cellular and Molecular Medicine,
Journal Year:
2025,
Volume and Issue:
29(9)
Published: May 1, 2025
ABSTRACT
Hepatopulmonary
syndrome
(HPS)
is
a
pulmonary
vascular
complication
of
liver
disease
and/or
portal
hypertension.
HPS
manifests
as
impaired
gas
exchange
and
hypoxemia
due
to
intrapulmonary
dilatations
shunts.
In
response
primary
disease,
the
abnormal
adaptation
respiratory
epithelial
cells,
endothelial
cells
immune
leads
microenvironment
disequilibrium
HPS.
this
review,
we
explore
pathophysiologic
mechanisms
HPS,
including
dilation,
angiogenesis
alveolar
dysfunction.
The
contributor
transplantation
only
treatment
that
generally
reverses
We
then
discuss
how
disruption
hepatic
sinusoidal
homeostasis
may
impact
progression
mainly
focusing
on
hepatocytes,
cholangiocytes,
LSECs
macrophages.
As
occurs
more
commonly
in
advanced
cirrhosis,
also
normalisation
dysfunction
hypertension
crucial
for
resolution
conclusion,
liver‐targeted
therapies
be
effective
treating
Language: Английский