Alimentary Pharmacology & Therapeutics,
Journal Year:
2024,
Volume and Issue:
60(5), P. 662 - 663
Published: July 30, 2024
LINKED
CONTENT
This
article
is
linked
to
Bansal
et
al.
papers.
To
view
these
articles,
visit
https://doi.org/10.1111/apt.17930
and
https://doi.org/10.1111/apt.18124
.
Advanced Science,
Journal Year:
2025,
Volume and Issue:
unknown
Published: May 8, 2025
Abstract
Conjugated
lithocholic
acid
(LCA)
plays
a
critical
role
in
the
development
of
metabolic
dysfunction‐associated
steatotic
liver
disease
(MASLD).
In
this
process,
hepatocyte
inflammation‐caused
upregulation
its
receptor,
Takeda
G
protein‐coupled
receptor
5
(TGR5)
is
crucial
factor.
Serum
bile
profiling
shows
an
increase
conjugated
LCA,
which
correlates
with
severity.
Depletion
Gpbar1
hepatocytes
significantly
protects
against
progression
from
MASLD
to
steatohepatitis
(MASH)
that
related
LCA.
vivo
and
vitro
experiments
indicate
TGR5
activation
promotes
lipotoxicity‐induced
cell
death
inflammation
by
suppressing
de
novo
carnitine
biosynthesis.
Mechanistically,
binding
CD36
facilitates
E3
ubiquitin
ligase
TRIM21
recruitment,
leading
degradation
BBOX1,
enzyme
Targeting
therapeutically
can
restore
biosynthesis,
may
offer
potent
strategy
prevent
or
reverse
transition
MASH.
Alimentary Pharmacology & Therapeutics,
Journal Year:
2024,
Volume and Issue:
60(5), P. 660 - 661
Published: July 30, 2024
LINKED
CONTENT
This
article
is
linked
to
Lin
et
al
papers.
To
view
these
articles,
visit
https://doi.org/10.1111/apt.17930
and
https://doi.org/10.1111/apt.18182
.
Alimentary Pharmacology & Therapeutics,
Journal Year:
2024,
Volume and Issue:
60(5), P. 662 - 663
Published: July 30, 2024
LINKED
CONTENT
This
article
is
linked
to
Bansal
et
al.
papers.
To
view
these
articles,
visit
https://doi.org/10.1111/apt.17930
and
https://doi.org/10.1111/apt.18124
.