Key genes and pathways in asparagine metabolism in Alzheimer’s Disease: a bioinformatics approach
Xiaoqian Lan,
No information about this author
Guangli Feng,
No information about this author
Qing Li
No information about this author
et al.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 28, 2025
Abstract
Background
Asparagine
(Asn)
metabolism
is
essential
for
maintaining
cellular
homeostasis
and
supporting
neuronal
energy
demands.
Recent
studies
have
suggested
its
dysregulation
may
contribute
to
Alzheimer’s
disease
(AD)
pathogenesis;
however,
the
specific
genes
regulatory
mechanisms
involved
remain
incompletely
understood.
Methods
Four
publicly
available
microarray
datasets
(GSE5281,
GSE29378,
GSE36980,
GSE138260)
were
utilized
investigate
with
differential
expression
between
control
AD
samples.
metabolism-related
(AMGs)
retrieved
from
GeneCards
database,
their
intersection
DEGs
yielded
candidate
asparagine
differentially
expressed
(AMG-DEGs).
Functional
enrichment
analysis
(Gene
Set
Enrichment
Analysis,
Gene
Ontology
Kyoto
Encyclopedia
of
Genes
Genomes),
protein–protein
interaction
(PPI)
network
analysis,
centrality
scoring
identified
hub
genes.
Regulatory
investigated
through
construction
competing
endogenous
RNA
transcription
factor
networks.
Potential
therapeutic
compounds
predicted
via
drug–gene
evaluated
using
molecular
docking
simulations.
Results
Thirty-nine
AMG-DEGs
found
be
enriched
in
neurodevelopmental,
synaptic
transmission,
inflammatory
signaling
pathways.
PPI
screening
revealed
seven
(
HPRT1
,
GAD2
TUBB3
GFAP
CD44
CCL2
NFKBIA
).
highlighted
miRNAs,
long
non-coding
RNAs,
factors
modulation.
Drug
Bathocuproine
disulfonate,
DL-Mevalonic
acid,
Phenethyl
isothiocyanate
as
promising
strong
binding
affinities
proteins.
Conclusion
This
study
comprehensively
maps
reveals
a
set
elements
potentially
progression.
The
provide
foundation
further
experimental
validation
development
novel
metabolism-targeted
strategies
treatment.
Language: Английский
Chronic Inflammation and Immune Dysregulation in Metabolic-Dysfunction-Associated Steatotic Liver Disease Progression: From Steatosis to Hepatocellular Carcinoma
Young-min Jee,
No information about this author
Jeong‐Yoon Lee,
No information about this author
Tom Ryu
No information about this author
et al.
Biomedicines,
Journal Year:
2025,
Volume and Issue:
13(5), P. 1260 - 1260
Published: May 21, 2025
Background/Objectives:
Metabolic-dysfunction-associated
steatotic
liver
disease
(MASLD)
progresses
from
hepatic
steatosis
to
hepatocellular
carcinoma
(HCC)
as
a
result
of
systemic
immunometabolic
dysfunction.
This
review
summarizes
the
key
roles
innate
and
adaptive
immune
mechanisms
driving
injury,
fibrogenesis,
carcinogenesis
in
MASLD.
Methods:
A
comprehensive
literature
was
performed
using
PubMed
identify
relevant
published
studies.
Eligible
articles
included
original
research
clinical
studies
addressing
immunological
metabolic
MASLD,
well
emerging
therapeutic
strategies.
Results:
We
highlight
cytokine
networks,
gut–liver
axis,
cell
reprogramming.
Emerging
strategies,
including
inhibitors,
anti-fibrotic
agents,
modulators,
nutraceuticals,
offer
several
indications
for
attenuating
MASLD
progression
reducing
prevalence
extrahepatic
manifestations.
Conclusions:
Given
heterogeneity
personalized
combination-based
approaches
targeting
both
inflammation
stress
are
essential
effective
management
prevention
complications.
Language: Английский