SLC25A37 is casually associated with the increased incidence of benign prostatic hyperplasia

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Abstract The etiology of benign prostatic hyperplasia (BPH) remains unclear. Here, we conducted a combined analysis integrating single-cell RNA sequencing (scRNA-seq) and Mendelian randomization (MR) to reveal the causal effect of potential genes associated with the incidence of BPH. Based on scRNA-seq, we found the number of monocytes increased in prostate transition zone tissues of BPH patients and analyzed the differentially expressed genes (DEGs) specific to monocytes. We identified SLC25A37, a member of solute carrier transporters, was casually associated with increased incidence of BPH based on MR, Bayesian colocalization, and reverse MR analyses. Follow-up analysis showed SLC25A37 was involved in inflammation and cell proliferation-related signaling pathways in classical monocytes in prostate transition zone tissues. We also revealed the potential associations between the SLC25A37 gene and BPH pathogenic genes, current BPH drug targets, as well as the patient’s age, providing novel insights into the underlying mechanism and potential therapeutic options of BPH.
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SLC25A37 is casually associated with the increased incidence of benign prostatic hyperplasia | 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 SLC25A37 is casually associated with the increased incidence of benign prostatic hyperplasia Wei Xue, Zhen Tong, Wei Zhang, Xinrui Wu, Xinxing Du, Zehong Peng, and 1 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-3850747/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract The etiology of benign prostatic hyperplasia (BPH) remains unclear. Here, we conducted a combined analysis integrating single-cell RNA sequencing (scRNA-seq) and Mendelian randomization (MR) to reveal the causal effect of potential genes associated with the incidence of BPH. Based on scRNA-seq, we found the number of monocytes increased in prostate transition zone tissues of BPH patients and analyzed the differentially expressed genes (DEGs) specific to monocytes. We identified SLC25A37, a member of solute carrier transporters, was casually associated with increased incidence of BPH based on MR, Bayesian colocalization, and reverse MR analyses. Follow-up analysis showed SLC25A37 was involved in inflammation and cell proliferation-related signaling pathways in classical monocytes in prostate transition zone tissues. We also revealed the potential associations between the SLC25A37 gene and BPH pathogenic genes, current BPH drug targets, as well as the patient’s age, providing novel insights into the underlying mechanism and potential therapeutic options of BPH. Health sciences/Urology/Prostate Health sciences/Diseases/Urogenital diseases/Urinary tract obstruction Full Text Additional Declarations There is NO Competing Interest. Supplementary Files Supplementarydata.xlsx Cite Share Download PDF Status: Posted 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. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. 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