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Serum protein quantitative trait loci, human single-cell ocular atlases, and UK Biobank macular optical coherence tomography (OCT) imaging were used for downstream analyses.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Study Selection<\/jats:title>\n                  <jats:p>Five European-ancestry cohorts with genome-wide data and cohort-specific CSC case-control definitions were included, comprising 2,584 cases and 1,044,455 controls. Variants present in at least 2 cohorts were meta-analyzed.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Data Extraction and Synthesis<\/jats:title>\n                  <jats:p>Cohort-level GWASs were adjusted for age, age squared, sex, genotyping array or batch, and 10 genetic principal components, then combined using fixed-effects inverse-variance meta-analysis. Post-GWAS analyses included gene prioritization, colocalization, Mendelian randomization, single-cell disease-relevance scoring, and testing of a CSC genetic risk score in UK Biobank OCT images.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Main Outcome(s) and Measure(s)<\/jats:title>\n                  <jats:p>Genome-wide significant CSC loci, effector genes and proteins, tissue and cell-type enrichment, and CSC-relevant OCT abnormalities.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>\n                    Across 11,068,938 variants, 10 loci reached genome-wide significance (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 5 \u00d7 10\u22128), including 3 novel loci near\n                    <jats:italic>TGFB1, LINC00551<\/jats:italic>\n                    , and\n                    <jats:italic>LOC105375630<\/jats:italic>\n                    and 7 replicated loci near\n                    <jats:italic>CFH, CD46, NOTCH4, PREX1, PTPRB, GATA5<\/jats:italic>\n                    , and\n                    <jats:italic>TNFRSF10A<\/jats:italic>\n                    . Integrative analyses prioritized 10 candidate effector genes. Colocalization and Mendelian randomization implicated circulating TNFRSF10A, TGFB1, and CASP10 levels. Single-cell analyses localized genetic risk to sclera (\n                    <jats:italic>P<\/jats:italic>\n                    = 2.0 \u00d7 10\u22124) and vascular endothelial cells (\n                    <jats:italic>P<\/jats:italic>\n                    = 4.0 \u00d7 10\u22124), with fibroblast enrichment. In UK Biobank, OCT abnormalities were more frequent in the top vs bottom 1% of CSC genetic risk (18 of 109 [16.5%] vs 8 of 134 [6.0%]; odds ratio, 4.05; 95% CI, 1.65-10.87;\n                    <jats:italic>P<\/jats:italic>\n                    = .002).\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Conclusions and Relevance<\/jats:title>\n                  <jats:p>In this GWAS meta-analysis, CSC susceptibility localized predominantly to scleral and vascular biology rather than primary retinal pigment epithelial dysfunction. These findings support CSC as a sclerovascular disorder and nominate complement regulation, endothelial signaling, and extracellular matrix pathways for future study.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Key Points<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Question<\/jats:title>\n                    <jats:p>What genetic loci, genes, proteins, and ocular cell types underlie susceptibility to central serous chorioretinopathy (CSC)?<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Findings<\/jats:title>\n                    <jats:p>In this GWAS meta-analysis of 2,584 CSC cases and 1,044,455 controls, 10 genome-wide significant loci were identified, including 3 novel loci. Integrative analyses implicated scleral fibroblasts and vascular endothelial cells, prioritized candidate effector genes and circulating proteins, and showed that high CSC genetic risk was associated with more frequent RPE abnormalities on macular OCT.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Meaning<\/jats:title>\n                    <jats:p>These findings support CSC as a primary sclerovascular disorder and nominate mechanism-linked pathways for future translational studies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Importance<\/jats:title>\n                    <jats:p>The primary site of dysfunction in central serous chorioretinopathy (CSC) remains uncertain.<\/jats:p>\n                  <\/jats:sec>\n                <\/jats:sec>","DOI":"10.64898\/2026.05.20.26353693","type":"posted-content","created":{"date-parts":[[2026,5,23]],"date-time":"2026-05-23T01:40:24Z","timestamp":1779500424000},"source":"Crossref","is-referenced-by-count":0,"title":["GWAS Meta-analysis Identifies Novel Associated Loci and Points to Causal Tissues in Central Serous Chorioretinopathy"],"prefix":"10.64898","author":[{"given":"Liyin","family":"Chen","sequence":"first","affiliation":[{"name":"Harvard Medical School Department of Ophthalmology, Massachusetts Eye and Ear, Boston, MA, USA"},{"name":"Broad Institute of MIT and Harvard, Cambridge, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Soo Hyun","family":"Kim","sequence":"additional","affiliation":[{"name":"Harvard Medical School Department of Ophthalmology, Massachusetts Eye and Ear, Boston, MA, USA"},{"name":"Broad Institute of MIT and Harvard, Cambridge, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Buu","family":"Truong","sequence":"additional","affiliation":[{"name":"Broad Institute of MIT and Harvard, Cambridge, MA, USA"},{"name":"Heart and Vascular Institute and Center for Genomic Medicine, Mass General Brigham, Boston, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joel T","family":"R\u00e4m\u00f6","sequence":"additional","affiliation":[{"name":"Institute for Molecular Medicine Finland (FIMM), Helsinki Institute of Life Science (HiLIFE), University of Helsinki, Helsinki, Finland"},{"name":"Massachusetts Eye and Ear, Boston, MA, USA"},{"name":"Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bryan R","family":"Gorman","sequence":"additional","affiliation":[{"name":"Center for Data and Computational Sciences (C-DACS), VA Boston Healthcare System, Boston, MA, USA"},{"name":"Booz Allen Hamilton, McLean, VA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elon H. 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