Genomic Structural Equation Modeling Elucidates the Shared Genetic Architecture of Allergic Disorders
Research Square (Research Square),
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 1, 2025
Abstract
Background
The
intricate
shared
genetic
architecture
underlying
allergic
disorders—including
asthma,
atopic
dermatitis,
contact
rhinitis,
conjunctivitis,
urticaria,
anaphylaxis,
and
eosinophilic
esophagitis—remains
incompletely
characterized.
Methods
Our
study
employed
genomic
structural
equation
modeling
(Genomic
SEM)
to
define
the
common
factor
representing
of
disorders.
Coupled
with
diverse
post-GWAS
analytical
methods,
we
aimed
discover
susceptible
loci
investigate
associations
external
traits.
Furthermore,
explored
enriched
pathways,
cellular
layers,
elements,
investigated
putative
plasma
protein
biomarkers.
Polygenic
risk
score
(PRS)
analyses,
leveraging
our
integrated
GWAS
data,
were
conducted
assess
chromosomal-level
for
Results
A
well-fitted
SEM
revealing
We
identified
a
total
2038
genome-wide
significant
SNP
(p
<
5e-8),
including
31
previously
unreported
loci.
Fine-mapping
variants
gene
sets
pinpointed
2
causal
candidate
genes.
Genetic
correlation
analyses
further
illuminated
multiple
traits,
notably
psychiatric
Preliminary
findings
four
Conclusion
Notably,
this
presents
first
comprehensive
characterization
disorders
through
analysis
an
unmeasured
composite
phenotype,
providing
novel
insights
into
etiological
pathways
across
these
conditions.
Язык: Английский
Genomic structural equation modeling elucidates the shared genetic architecture of allergic disorders
Journal of Translational Medicine,
Год журнала:
2025,
Номер
23(1)
Опубликована: Апрель 15, 2025
The
intricate
shared
genetic
architecture
underlying
allergic
disorders-including
asthma,
atopic
dermatitis,
contact
rhinitis,
conjunctivitis,
urticaria,
anaphylaxis,
and
eosinophilic
esophagitis-remains
incompletely
characterized.
Our
study
employed
genomic
structural
equation
modeling
(Genomic
SEM)
to
define
the
common
factor
representing
of
disorders.
Coupled
with
diverse
post-GWAS
analytical
methods,
we
aimed
discover
susceptible
loci
investigate
associations
external
traits.
Furthermore,
explored
enriched
pathways,
cellular
layers,
elements,
investigated
putative
plasma
protein
biomarkers.
Polygenic
risk
score
(PRS)
analyses,
leveraging
our
integrated
GWAS
data,
were
conducted
assess
chromosomal-level
for
A
well-fitted
SEM
revealing
We
identified
a
total
2038
genome-wide
significant
SNP
(p
<
5e-8),
including
31
previously
unreported
loci.
Fine-mapping
variants
gene
sets
pinpointed
2
causal
candidate
genes.
Genetic
correlation
analyses
further
illuminated
multiple
traits,
notably
psychiatric
Preliminary
findings
four
Notably,
this
presents
first
comprehensive
characterization
disorders
through
analysis
an
unmeasured
composite
phenotype,
providing
novel
insights
into
etiological
pathways
across
these
conditions.
Язык: Английский