{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,2]],"date-time":"2026-05-02T19:00:38Z","timestamp":1777748438435,"version":"3.51.4"},"reference-count":63,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"21","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2019,11,5]]},"abstract":"\n Background<\/jats:title>\n \n Inflammation and fibrosis play an important role in the pathogenesis of atrial fibrillation (\n AF<\/jats:styled-content>\n ) after myocardial infarction (\n MI<\/jats:styled-content>\n ). CTRP9 (C1q\/tumor necrosis factor\u2010related protein\u20109) as a secreted glycoprotein can reverse left ventricle remodeling post\u2010\n MI<\/jats:styled-content>\n , but its effects on\n MI<\/jats:styled-content>\n \u2010induced atrial inflammation, fibrosis, and associated\n AF<\/jats:styled-content>\n are unknown.\n <\/jats:p>\n <\/jats:sec>\n \n Methods and Results<\/jats:title>\n \n MI<\/jats:styled-content>\n model rats received adenoviral supplementation of\n CTRP<\/jats:styled-content>\n 9 (Ad\u2010\n CTRP<\/jats:styled-content>\n 9) by jugular\u2010vein injection. Cardiac function, inflammatory, and fibrotic indexes and related signaling pathways, electrophysiological properties, and\n AF<\/jats:styled-content>\n inducibility of atria in\u00a0vivo and ex\u00a0vivo were detected in 3 or 7\u00a0days after\n MI<\/jats:styled-content>\n . shCTRP9 (short hairpin CTRP9) and sh\n RNA<\/jats:styled-content>\n were injected into rat and performed similar detection at day 5 or 10. Adverse atrial inflammation and fibrosis, cardiac dysfunction were induced in both\n MI<\/jats:styled-content>\n and Ad\u2010GFP (adenovirus\u2010encoding green fluorescent protein)+\n MI<\/jats:styled-content>\n rats. Systemic\n CTRP<\/jats:styled-content>\n 9 treatment improved cardiac dysfunction post\u2010\n MI<\/jats:styled-content>\n .\n CTRP<\/jats:styled-content>\n 9 markedly ameliorated macrophage infiltration and attenuated the inflammatory responses by downregulating interleukin\u20101\u03b2 and interleukin\u20106, and upregulating interleukin\u201010, in 3\u00a0days post\u2010\n MI<\/jats:styled-content>\n ; depressed left atrial fibrosis by decreasing the expressions of collagen types I and\n III<\/jats:styled-content>\n , \u03b1\u2010\n SMA<\/jats:styled-content>\n , and transforming growth factor \u03b21 in 7\u00a0days post\u2010\n MI<\/jats:styled-content>\n possibly through depressing the Toll\u2010like receptor 4\/nuclear factor\u2010\u03baB and Smad2\/3 signaling pathways. Electrophysiologic recordings showed that increased\n AF<\/jats:styled-content>\n inducibility and duration, and prolongation of interatrial conduction time induced by\n MI<\/jats:styled-content>\n were attenuated by\n CTRP<\/jats:styled-content>\n 9; moreover,\n CTRP<\/jats:styled-content>\n 9 was negatively correlated with interleukin\u20101\u03b2 and\n AF<\/jats:styled-content>\n duration. Downregulation of\n CTRP<\/jats:styled-content>\n 9 aggravated atrial inflammation, fibrosis, susceptibility of\n AF<\/jats:styled-content>\n and prolonged interatrial conduction time, without affecting cardiac function.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n CTRP<\/jats:styled-content>\n 9 is effective at attenuating atrial inflammation and fibrosis, possibly via its inhibitory effects on the Toll\u2010like receptor 4\/nuclear factor\u2010\u03baB and Smad2\/3 signaling pathways, and may be an original upstream therapy for\n AF<\/jats:styled-content>\n in early phase of\n MI<\/jats:styled-content>\n .\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/jaha.119.013133","type":"journal-article","created":{"date-parts":[[2019,10,18]],"date-time":"2019-10-18T09:00:13Z","timestamp":1571389213000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":62,"title":["CTRP9 Ameliorates Atrial Inflammation, Fibrosis, and Vulnerability to Atrial Fibrillation in Post\u2010Myocardial Infarction Rats"],"prefix":"10.1161","volume":"8","author":[{"given":"Mingxin","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University Hubei China"},{"name":"Cardiovascular Research Institute of Wuhan University Hubei China"},{"name":"Hubei Key Laboratory of Cardiology Hubei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wei","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University Hubei China"},{"name":"Cardiovascular Research Institute of Wuhan University Hubei China"},{"name":"Hubei Key Laboratory of Cardiology Hubei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Huibo","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University Hubei China"},{"name":"Cardiovascular Research Institute of Wuhan University Hubei China"},{"name":"Hubei Key Laboratory of Cardiology Hubei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lin","family":"Yin","sequence":"additional","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University Hubei China"},{"name":"Cardiovascular Research Institute of Wuhan University Hubei China"},{"name":"Hubei Key Laboratory of Cardiology Hubei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bingjie","family":"Ye","sequence":"additional","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University Hubei China"},{"name":"Cardiovascular Research Institute of Wuhan University Hubei China"},{"name":"Hubei Key Laboratory of Cardiology Hubei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yanhong","family":"Tang","sequence":"additional","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University Hubei China"},{"name":"Cardiovascular Research Institute of Wuhan University Hubei China"},{"name":"Hubei Key Laboratory of Cardiology Hubei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Congxin","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University Hubei China"},{"name":"Cardiovascular Research Institute of Wuhan University Hubei China"},{"name":"Hubei Key Laboratory of Cardiology Hubei China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_1_2_2","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehi629"},{"key":"e_1_3_1_3_2","doi-asserted-by":"publisher","DOI":"10.1093\/europace\/euw344"},{"key":"e_1_3_1_4_2","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehn579"},{"key":"e_1_3_1_5_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.110.990192"},{"key":"e_1_3_1_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijcard.2009.05.065"},{"key":"e_1_3_1_7_2","first-page":"451","article-title":"New\u2010onset atrial fibrillation in settings of acute coronary syndrome","volume":"14","author":"Galjautdinov GS","year":"2018","unstructured":"Galjautdinov GS, Gorelkin IV, Ibragimova KR, Sadriev RR. 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