Selective blockade of microRNA-31-5p/calcitonin receptor interaction reverses established atrial fibrosis and atrial arrhythmia substrate

Selective blockade of microRNA-31-5p/calcitonin receptor interaction reverses established atrial fibrosis and atrial arrhythmia substrate | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Article Selective blockade of microRNA-31-5p/calcitonin receptor interaction reverses established atrial fibrosis and atrial arrhythmia substrate Jasha Trompf*, Kathryn Cox*, Mohit Hulsurkar*, Lucia M. Moreira, and 24 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8484728/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted You are reading this latest preprint version Abstract Atrial fibrillation (AF), the commonest cardiac arrhythmia, is a major contributor to mortality and morbidity. Atrial tissue fibrosis, a hallmark of structural remodelling in AF, is currently incurable and significantly hinders AF-treatment. MicroRNA(miR)-31 is linked to ageing (a key risk factor for AF). Here, we show that AF-patients are characterised by upregulation of miR-31-5p in atrial cardiofibroblasts that negatively regulates the calcitonin receptor (CTR), thereby promoting atrial fibrogenesis and arrhythmia. Specific blockade of miR-31-5p/CTR-mRNA binding with LNA-miRNA-Target-Site-Blocker selectively increases atrial CTR expression and reverses advanced atrial fibrosis and arrhythmogenesis in vivo. These findings suggest a key role for miR-31-5p/CTR binding in promoting atrial fibrosis and arrhythmogenesis, and represents a first example of an RNA-based therapeutic capable of reversing established fibrosis that forms an AF substrate. *Jasha Trompf, Kathryn Cox, and Mohit Hulsurkar contributed equally to this work. Biological sciences/Cell biology/Cell signalling Biological sciences/Molecular biology/Non-coding RNAs Full Text Additional Declarations There is NO Competing Interest. Supplementary Files EXCELFILEWB.xlsx WB source data SUPPLEMENTARYMATERIALS.docx Supplementry material. Cite Share Download PDF Status: Under Review Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-8484728","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Article","associatedPublications":[],"authors":[{"id":569376940,"identity":"09ea3e4b-7be1-466f-89a5-b00ea6dbead2","order_by":0,"name":"Jasha Trompf*","email":"","orcid":"","institution":"Division of Cardiovascular Medicine, Radcliffe Department of Medicine, British Heart Foundation Centre of Research Excellence, University of Oxford, John Radcliffe Hospital, Oxford, OX3 9DU, UK","correspondingAuthor":false,"prefix":"","firstName":"Jasha","middleName":"","lastName":"Trompf*","suffix":""},{"id":569376941,"identity":"c304593b-97e6-430a-a882-615ecd2e85d3","order_by":1,"name":"Kathryn Cox*","email":"","orcid":"","institution":"Division of Cardiovascular Medicine, Radcliffe Department of Medicine, British Heart Foundation Centre of Research Excellence, University of Oxford, John Radcliffe Hospital, Oxford, OX3 9DU, UK","correspondingAuthor":false,"prefix":"","firstName":"Kathryn","middleName":"","lastName":"Cox*","suffix":""},{"id":569376942,"identity":"5696a57a-0665-45fc-998d-d51b6add6a1b","order_by":2,"name":"Mohit Hulsurkar*","email":"","orcid":"","institution":"Cardiovascular Research Institute, Baylor College of Medicine, One Baylor Plaza BCM335, Houston, USA; Department of Integrative Physiology, Baylor College of Medicine, One Baylor Plaza BCM335, Houston, USA","correspondingAuthor":false,"prefix":"","firstName":"Mohit","middleName":"","lastName":"Hulsurkar*","suffix":""},{"id":569376943,"identity":"c3775095-3cbb-46cd-86c4-4756926c4550","order_by":3,"name":"Lucia M. 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Atrial tissue fibrosis, a hallmark of structural remodelling in AF, is currently incurable and significantly hinders AF-treatment. MicroRNA(miR)-31 is linked to ageing (a key risk factor for AF). Here, we show that AF-patients are characterised by upregulation of miR-31-5p in atrial cardiofibroblasts that negatively regulates the calcitonin receptor (CTR), thereby promoting atrial fibrogenesis and arrhythmia. Specific blockade of miR-31-5p/CTR-mRNA binding with LNA-miRNA-Target-Site-Blocker selectively increases atrial CTR expression and reverses advanced atrial fibrosis and arrhythmogenesis in vivo. These findings suggest a key role for miR-31-5p/CTR binding in promoting atrial fibrosis and arrhythmogenesis, and represents a first example of an RNA-based therapeutic capable of reversing established fibrosis that forms an AF substrate.\u003c/p\u003e\n\u003cp\u003e\u003cbr\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e*Jasha Trompf, Kathryn Cox, and Mohit Hulsurkar contributed equally to this work.\u003c/strong\u003e\u003c/p\u003e","manuscriptTitle":"Selective blockade of microRNA-31-5p/calcitonin receptor interaction reverses established atrial fibrosis and atrial arrhythmia substrate","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-01-07 03:28:35","doi":"10.21203/rs.3.rs-8484728/v1","editorialEvents":[],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"nature-cardiovascular-research","isNatureJournal":true,"hasQc":false,"allowDirectSubmit":false,"externalIdentity":"natcardiovascres","sideBox":"Learn more about [Nature Cardiovascular Research](https://www.nature.com/natcardiovascres/)","snPcode":"","submissionUrl":"https://mts-natcardiovascres.nature.com/cgi-bin/main.plex","title":"Nature Cardiovascular Research","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"ejp","reportingPortfolio":"Nature Research","inReviewEnabled":true,"inReviewRevisionsEnabled":false}}],"origin":"","ownerIdentity":"63309ec4-fbf3-4b93-bc64-6cdce8753e0e","owner":[],"postedDate":"January 7th, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[{"id":60580921,"name":"Biological sciences/Cell biology/Cell signalling"},{"id":60580922,"name":"Biological sciences/Molecular biology/Non-coding RNAs"}],"tags":[],"updatedAt":"2026-04-16T14:46:34+00:00","versionOfRecord":[],"versionCreatedAt":"2026-01-07 03:28:35","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8484728","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8484728","identity":"rs-8484728","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}