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Despite the substantial health burden presented by chronic dry cough, its biological mechanisms remain unclear. We hypothesised shared genetic architecture between chronic dry cough and ACEi-induced cough and aimed to identify causal genes underlying both phenotypes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We performed multi-ancestry genome-wide association studies (GWAS) of chronic dry cough and ACEi-induced cough, and a multi-trait GWAS of both phenotypes, utilising data from five cohort studies. Chronic dry cough was defined by questionnaire responses, and ACEi-induced cough by treatment switches or clinical diagnosis in electronic health records. We mapped putative causal genes and performed phenome-wide association studies (PheWAS) of associated variants, and polygenic scores for ACEi-induced cough, to identify pleiotropic effects.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We found seven novel genetic association signals reaching p&lt;5\u00d710\n                      <jats:sup>\u20138<\/jats:sup>\n                      in the multi-trait or single-trait analyses of chronic dry cough and ACEi-induced cough. The novel variants mapped to 10 novel genes, and we mapped an additional three novel genes to known risk variants, many of which implicate neurological functions (\n                      <jats:italic>CTNNA1<\/jats:italic>\n                      ,\n                      <jats:italic>KCNA10<\/jats:italic>\n                      ,\n                      <jats:italic>MAPKAP1<\/jats:italic>\n                      ,\n                      <jats:italic>OR4C12<\/jats:italic>\n                      ,\n                      <jats:italic>OR4C13<\/jats:italic>\n                      ,\n                      <jats:italic>SIL1<\/jats:italic>\n                      ). The polygenic-score-based PheWAS highlighted associations with an elevated risk of several clinical conditions including asthma, diabetes and multi-site chronic pain.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our findings provide support for neuronal dysfunction underlying cough hypersensitivity in chronic dry cough and ACEi-induced cough, and identify diseases and traits associated with genetic predisposition to cough that could inform drug target discovery.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1183\/13993003.02341-2024","type":"journal-article","created":{"date-parts":[[2025,7,17]],"date-time":"2025-07-17T15:15:19Z","timestamp":1752765319000},"page":"2402341","update-policy":"https:\/\/doi.org\/10.1183\/ers-crossmark-policy","source":"Crossref","is-referenced-by-count":14,"title":["Genomics of chronic dry cough unravels 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