SynthesisEBioMedicine2025
Common and rare variant analyses reveal genetic factors underlying idiopathic pulmonary fibrosis and its shared aetiology with severe COVID-19.
Synthesis in EBioMedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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23 authors.
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Abstract
backgroundIdiopathic pulmonary fibrosis (IPF) is a progressive and debilitating respiratory disease with limited therapeutic options. Genetic association studies for IPF have identified several associations and probable effector genes that could not only help understanding IPF pathogenesis but also develop effective treatments. Assessing genetic overlap between IPF and severe COVID-19, an acute respiratory disease that can trigger pulmonary fibrosis, may reveal shared aetiology and mechanisms, thereby supporting the development of common treatments.
methodsWe carried out genome-wide association studies (GWAS), post-GWAS, and rare variant analyses using whole genome sequencing data from the 100,000 Genomes Project IPF cohort (n = 586). We performed a meta-analysis combining 100 kGP with published IPF GWASs (total 11,746 cases and 1,416,493 controls). We tested inhibition in vitro for a probable effector gene of an identified association. We also investigated genetic colocalisation between IPF and severe COVID-19 and leveraged their genetic correlation through multi-trait meta-analysis for discovery.
findingsIPF meta-analysis identified an additional association at 1q21.2 (rs16837903, OR [95% CI] = 0.88 [0.85, 0.92], P = 9.5 × 10
interpretationThese findings prioritise probable effector genes mediating IPF risk and identify potential therapeutic targets that require validation, with genes colocalising with severe COVID-19 suggesting potential for developing common treatments.
fundingNone.
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