@article {9576,
	title = {{Genome-wide association study of preserved ratio impaired spirometry (PRISm)},
	journal = {Eur Respir J},
	volume = {63},
	year = {2024},
	month = {Jan},
	abstract = {{0.70. PRISm is associated with respiratory symptoms and comorbidities. Our objective was to discover novel genetic signals for PRISm and see if they provide insight into the pathogenesis of PRISm and associated comorbidities.\ We undertook a genome-wide association study (GWAS) of PRISm in UK Biobank participants (Stage 1), and selected single nucleotide polymorphisms (SNPs) reaching genome-wide significance for replication in 13 cohorts (Stage 2). A combined meta-analysis of Stage 1 and Stage 2 was done to determine top SNPs. We used cross-trait linkage disequilibrium score regression to estimate genome-wide genetic correlation between PRISm and pulmonary and extrapulmonary traits. Phenome-wide association studies of top SNPs were performed.\ =0.12},
	author = {Higbee, D. H. and Lirio, A. and Hamilton, F. and Granell, R. and Wyss, A. B. and London, S. J. and Bartz, T. M. and Gharib, S. A. and Cho, M. H. and Wan, E. and Silverman, E. and Crapo, J. D. and Lominchar, J. V. T. and Hansen, T. and Grarup, N. and Dantoft, T. and rhus, L. and Linneberg, A. and O{\textquoteright}Connor, G. T. and Dupuis, J. and Xu, H. and De Vries, M. M. and Hu, X. and Rich, S. S. and Barr, R. G. and Manichaikul, A. and Wijnant, S. R. A. and Brusselle, G. G. and Lahousse, L. and Li, X. and ndez Cordero, A. I. and Obeidat, M. and Sin, D. D. and Harris, S. E. and Redmond, P. and Taylor, A. M. and Cox, S. R. and Williams, A. T. and Shrine, N. and John, C. and Guyatt, A. L. and Hall, I. P. and Davey Smith, G. and Tobin, M. D. and Dodd, J. W.}
}
@article {9863,
	title = {{Multi-ancestry genome-wide association study reveals novel genetic signals for lung function decline},
	journal = {medRxiv},
	year = {2024},
	month = {Nov},
	abstract = {Accelerated decline in lung function contributes to the development of chronic respiratory disease. Despite evidence for a genetic component, few genetic associations with lung function decline have been identified.\ To evaluate genome-wide associations and putative downstream functionality of genetic variants with lung function decline in diverse general population cohorts.\ /FVC) in participants across six cohorts in the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium and the UK Biobank. Genotypes were imputed to TOPMed (CHARGE cohorts) or Haplotype Reference Consortium (HRC) (UK Biobank) reference panels, and GWAS analyses used generalized estimating equation models with robust standard error. Models were stratified by cohort, ancestry, and sex, and adjusted for important lung function confounders and genotype principal components. Results were combined in cross-ancestry and ancestry-specific meta-analyses. Selected top variants were tested for replication in two independent COPD-enriched cohorts.\ ) with consistent associations across ancestries or decline phenotypes. Annotation class analysis revealed significant enrichment of several regulatory processes for corticosteroid biosynthesis and metabolism. Drug repurposing analysis identified 43 approved compounds targeting eight of the implicated 38 genes.\ Our multi-ancestry GWAS meta-analyses identified numerous genetic loci associated with lung function decline. These findings contribute knowledge to the genetic architecture of lung function decline, provide evidence for a role of endogenous corticosteroids in the etiology of lung function decline, and identify drug targets that merit further study for potential repurposing to slow lung function decline and treat lung disease.},
	author = {Patchen, B. K. and Zhang, J. and Gaddis, N. and Bartz, T. M. and Chen, J. and Debban, C. and Leonard, H. and Nguyen, N. Q. and Seo, J. and Tern, C. and Allen, R. and DeMeo, D. L. and Fornage, M. and Melbourne, C. and Minto, M. and Moll, M. and O{\textquoteright}Connor, G. and Pottinger, T. and Psaty, B. M. and Rich, S. S. and Rotter, J. I. and Silverman, E. K. and Stratford, J. and Graham Barr, R. and Cho, M. H. and Gharib, S. A. and Manichaikul, A. and North, K. and Oelsner, E. C. and Simonsick, E. M. and Tobin, M. D. and Yu, B. and Choi, S. H. and Dupuis, J. and Cassano, P. A. and Hancock, D. B.}
}
