Department of Ophthalmology, Amsterdam University Medical Center (AMC), Amsterdam, the Netherlands; Department of Clinical Genetics, Amsterdam University Medical Center (AMC), Amsterdam, the Netherlands; Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA; Institute for Quantitative and Computational Biosciences, David Geffen School of Medicine, UCLA, Los Angeles, CA, USA.
Cell Rep Med. 2024 Feb 20;5(2):101430. doi: 10.1016/j.xcrm.2024.101430.
Primary open-angle glaucoma (POAG), a leading cause of irreversible blindness globally, shows disparity in prevalence and manifestations across ancestries. We perform meta-analysis across 15 biobanks (of the Global Biobank Meta-analysis Initiative) (n = 1,487,441: cases = 26,848) and merge with previous multi-ancestry studies, with the combined dataset representing the largest and most diverse POAG study to date (n = 1,478,037: cases = 46,325) and identify 17 novel significant loci, 5 of which were ancestry specific. Gene-enrichment and transcriptome-wide association analyses implicate vascular and cancer genes, a fifth of which are primary ciliary related. We perform an extensive statistical analysis of SIX6 and CDKN2B-AS1 loci in human GTEx data and across large electronic health records showing interaction between SIX6 gene and causal variants in the chr9p21.3 locus, with expression effect on CDKN2A/B. Our results suggest that some POAG risk variants may be ancestry specific, sex specific, or both, and support the contribution of genes involved in programmed cell death in POAG pathogenesis.
原发性开角型青光眼(POAG)是全球导致不可逆性失明的主要原因,在不同种族中的患病率和表现存在差异。我们对 15 个生物库(全球生物库荟萃分析倡议)(n=1487441 例:病例=26848 例)进行了荟萃分析,并与以前的多种族研究合并,合并数据集代表了迄今为止最大和最多样化的 POAG 研究(n=1478037 例:病例=46325 例),并确定了 17 个新的显著位点,其中 5 个具有种族特异性。基因富集和转录组全关联分析提示血管和癌症基因,其中五分之一与原发性纤毛相关。我们在人类 GTEx 数据和大型电子健康记录中对 SIX6 和 CDKN2B-AS1 基因座进行了广泛的统计分析,结果显示 SIX6 基因与 chr9p21.3 基因座中的因果变异之间存在相互作用,对 CDKN2A/B 的表达有影响。我们的研究结果表明,一些 POAG 风险变异可能具有种族特异性、性别特异性或两者兼而有之,并支持参与程序性细胞死亡的基因在 POAG 发病机制中的作用。