rs11172406 - ATP23 - RN7SKP65
Magnitude 2.2 · 1 study on file
Reported associations
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Genomics of chronic dry cough unravels neurological pathways - Unknown journal (n.d.) · Unknown authors · PubMed 40675770
ABSTRACT: Graphical abstract Overview of the study. GWAS: genome-wide association study; ACEi: angiotensin-converting enzyme inhibitor. Background Chronic dry cough is a symptom of common lung conditions, can occur as a side-effect of angiotensin-converting enzyme inhibitors (ACEis), or may be unexplained. 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. Methods 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 wa
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Lifestyle context
Concrete actions anchored to the cited research. We do not prescribe, we describe.
Drug interactions
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ACE inhibitor-induced cough risk Moderate
Variants in ATP23 affect neuronal signaling pathways, increasing susceptibility to ACE inhibitor-induced dry cough through cough hypersensitivity mechanisms.
Discuss increased cough risk with your doctor; request ARB alternative if cough develops