{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T16:40:50Z","timestamp":1790181650675,"version":"4.1.0"},"reference-count":34,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2020,6,2]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Atrial tissue fibrosis is linked to inflammatory cells, yet is incompletely understood. A growing body of literature associates peripheral blood levels of the antifibrotic hormone BNP (B\u2010type natriuretic peptide) with atrial fibrillation (\n              <jats:styled-content style=\"fixed-case\">AF<\/jats:styled-content>\n              ). We investigated the relationship between pro\u2010fibrotic tissue M2 macrophage marker Cluster of Differentiation (\n              <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n              )163+, atrial procollagen expression, and\n              <jats:styled-content style=\"fixed-case\">BNP<\/jats:styled-content>\n              gene expression in patients with and without\n              <jats:styled-content style=\"fixed-case\">AF<\/jats:styled-content>\n              .\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              In a cross\u2010sectional study design, right atrial tissue was procured from 37 consecutive, consenting, stable patients without heart failure or left ventricular systolic dysfunction, of whom 10 had\n              <jats:styled-content style=\"fixed-case\">AF<\/jats:styled-content>\n              and 27 were non\u2010\n              <jats:styled-content style=\"fixed-case\">AF<\/jats:styled-content>\n              controls. Samples were analyzed for\n              <jats:styled-content style=\"fixed-case\">BNP<\/jats:styled-content>\n              and fibro\u2010inflammatory gene expression, as well as fibrosis and\n              <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n              163+. Primary analyses showed strong correlations (all\n              <jats:italic>P<\/jats:italic>\n              &lt;0.008) between M2 macrophage\n              <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n              163+ staining, procollagen gene expression, and myocardial\n              <jats:styled-content style=\"fixed-case\">BNP<\/jats:styled-content>\n              gene expression across the entire cohort. In secondary analyses without multiplicity adjustments,\n              <jats:styled-content style=\"fixed-case\">AF<\/jats:styled-content>\n              patients had greater left atrial volume index, more valve disease, higher serum\n              <jats:styled-content style=\"fixed-case\">BNP<\/jats:styled-content>\n              , and altered collagen turnover markers versus controls (all\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05).\n              <jats:styled-content style=\"fixed-case\">AF<\/jats:styled-content>\n              patients also showed higher atrial tissue M2 macrophage\n              <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n              163+, collagen volume fraction, gene expression of procollagen 1 and 3, as well as reduced expression of the\n              <jats:styled-content style=\"fixed-case\">BNP<\/jats:styled-content>\n              clearance receptor\n              <jats:styled-content style=\"fixed-case\">NPRC<\/jats:styled-content>\n              (all\n              <jats:italic>P<\/jats:italic>\n              &lt;0.05). Atrial procollagen 3 gene expression was correlated with fibrosis and\n              <jats:styled-content style=\"fixed-case\">BNP<\/jats:styled-content>\n              gene expression was correlated with serum\n              <jats:styled-content style=\"fixed-case\">BNP<\/jats:styled-content>\n              .\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Elevated atrial tissue pro\u2010fibrotic M2 macrophage\n              <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n              163+ is associated with increased myocardial gene expression of procollagen and anti\u2010fibrotic\n              <jats:styled-content style=\"fixed-case\">BNP<\/jats:styled-content>\n              and is higher in patients with\n              <jats:styled-content style=\"fixed-case\">AF<\/jats:styled-content>\n              . More work on modulation of\n              <jats:styled-content style=\"fixed-case\">BNP<\/jats:styled-content>\n              signaling for treatment and prevention of\n              <jats:styled-content style=\"fixed-case\">AF<\/jats:styled-content>\n              may be warranted.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.119.013416","type":"journal-article","created":{"date-parts":[[2020,5,20]],"date-time":"2020-05-20T09:05:49Z","timestamp":1589965549000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":35,"title":["Atrial Tissue Pro\u2010Fibrotic M2 Macrophage Marker CD163+, Gene Expression of Procollagen and B\u2010Type Natriuretic Peptide"],"prefix":"10.1161","volume":"9","author":[{"given":"Chris J.","family":"Watson","sequence":"first","affiliation":[{"name":"Centre for Experimental Medicine Queen's University Belfast Belfast Northern Ireland"},{"name":"Chronic Cardiovascular Disease Management Unit and Heart Failure Unit St Vincent's Healthcare Group Dublin Ireland"},{"name":"School of Medicine UCD Conway Institute University College Dublin Dublin Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nadezhda","family":"Glezeva","sequence":"additional","affiliation":[{"name":"Chronic Cardiovascular Disease Management Unit and Heart Failure Unit St Vincent's Healthcare Group Dublin Ireland"},{"name":"School of Medicine UCD Conway Institute University College Dublin Dublin Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen","family":"Horgan","sequence":"additional","affiliation":[{"name":"Sidney Kimmel Medical College Thomas Jefferson University Philadelphia PA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joe","family":"Gallagher","sequence":"additional","affiliation":[{"name":"Chronic Cardiovascular Disease Management Unit and Heart Failure Unit St Vincent's Healthcare Group Dublin Ireland"},{"name":"School of Medicine UCD Conway Institute University College Dublin Dublin Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dermot","family":"Phelan","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine Cleveland Clinic Cleveland OH"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ken","family":"McDonald","sequence":"additional","affiliation":[{"name":"Chronic Cardiovascular Disease Management Unit and Heart Failure Unit St Vincent's Healthcare Group Dublin Ireland"},{"name":"School of Medicine UCD Conway Institute University College Dublin Dublin Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Tolan","sequence":"additional","affiliation":[{"name":"Cardiology Department Blackrock Clinic Dublin Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John","family":"Baugh","sequence":"additional","affiliation":[{"name":"School of Medicine UCD Conway Institute University College Dublin Dublin Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrick","family":"Collier","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine Cleveland Clinic Cleveland OH"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark","family":"Ledwidge","sequence":"additional","affiliation":[{"name":"Chronic Cardiovascular Disease Management Unit and Heart Failure Unit St Vincent's Healthcare Group Dublin Ireland"},{"name":"School of Medicine UCD Conway Institute University College Dublin Dublin Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_1_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0735-1097(00)00515-5"},{"key":"e_1_3_1_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2004.09.045"},{"key":"e_1_3_1_4_2","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2013.7588"},{"key":"e_1_3_1_5_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa031994"},{"key":"e_1_3_1_6_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.109.873265"},{"key":"e_1_3_1_7_2","doi-asserted-by":"publisher","DOI":"10.1253\/circj.CJ-16-0759"},{"key":"e_1_3_1_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jjcc.2014.08.003"},{"key":"e_1_3_1_9_2","doi-asserted-by":"publisher","DOI":"10.1136\/heartjnl-2016-310236"},{"key":"e_1_3_1_10_2","first-page":"370","article-title":"B\u2010type natriuretic peptide, disease progression and clinical outcomes in atrial fibrillation","volume":"05","author":"Inohara T","year":"2018","unstructured":"Inohara T, Kim S, Pieper K, Blanco RG, Allen LA, Fonarow GC, Gersh BJ, Ezekowitz MD, Kowey PR, Reiffel JA, et al. 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