{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,22]],"date-time":"2026-01-22T21:03:35Z","timestamp":1769115815991,"version":"3.49.0"},"reference-count":38,"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":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Cardiac fibrosis occurs because of disruption of the extracellular matrix network leading to myocardial dysfunction. Angiotensin\n              <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n              (Ang\n              <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n              ) has been implicated in the development of cardiac fibrosis. Recently, micro\n              <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n              s have been identified as an attractive target for therapeutic intervention in cardiac pathologies; however, the underlying mechanism of micro\n              <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n              s in cardiac fibrosis remains unclear. Next\u2010generation sequencing analysis identified a novel characterized microRNA, miR\u20101954, that was significantly reduced in AngII\u2010infused mice. The finding led us to hypothesize that deficiency of miR\u20101954 triggers cardiac fibrosis.\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              A transgenic mouse was created using \u03b1\u2010MHC (\u03b1\u2010myosin heavy chain) promoter and was challenged with\n              <jats:styled-content style=\"fixed-case\">AngII<\/jats:styled-content>\n              infusion. AngII induced cardiac hypertrophy and remodeling. The in\u00a0vivo overexpression of miR\u20101954 showed significant reduction in cardiac mass and blood pressure in AngII\u2010infused mice. Further analysis showed significant reduction in cardiac fibrotic genes, hypertrophy marker genes, and an inflammatory gene and restoration of a calcium\u2010regulated gene (Atp2a2 [ATPase sarcoplasmic\/endoplasmic reticulum Ca2+ transporting 2]; also known as\n              <jats:styled-content style=\"fixed-case\">SERCA<\/jats:styled-content>\n              2), but no changes were observed in apoptotic genes.\n              <jats:styled-content style=\"fixed-case\">THBS<\/jats:styled-content>\n              1 (thrombospondin 1) is indicated as a target gene for miR\u20101954.\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              Our findings provide evidence, for the first time, that miR\u20101954 plays a critical role in cardiac fibrosis by targeting\u00a0\n              <jats:styled-content style=\"fixed-case\">THBS<\/jats:styled-content>\n              1. We conclude that promoting the level of miR\u20101954 would be a promising strategy for the treatment of cardiac fibrosis.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.119.012880","type":"journal-article","created":{"date-parts":[[2019,10,23]],"date-time":"2019-10-23T09:02:10Z","timestamp":1571821330000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":24,"title":["Deficiency of MicroRNA miR\u20101954 Promotes Cardiac Remodeling and Fibrosis"],"prefix":"10.1161","volume":"8","author":[{"given":"Valorie","family":"Chiasson","sequence":"first","affiliation":[{"name":"Department of Medical Physiology Texas A&amp;M University Temple TX"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ana Paula Cremasco","family":"Takano","sequence":"additional","affiliation":[{"name":"Department of Medical Physiology Texas A&amp;M University Temple TX"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rakeshwar S.","family":"Guleria","sequence":"additional","affiliation":[{"name":"Department of Medical Physiology Texas A&amp;M University Temple TX"},{"name":"VISN 17 Center of Excellence on Returning War Veterans Waco TX"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sudhiranjan","family":"Gupta","sequence":"additional","affiliation":[{"name":"Department of Biology Baylor University Waco TX"},{"name":"Department of Medical Physiology Texas A&amp;M University Temple TX"},{"name":"VISN 17 Center of Excellence on Returning War Veterans Waco TX"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvq308"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1007\/s10741-012-9365-4"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1755-5922.2010.00228.x"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1139\/Y09-105"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1186\/1755-1536-5-15"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.22322"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00408663"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.109.137885"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrm2868"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature07242"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.107.163147"},{"key":"e_1_3_2_13_2","doi-asserted-by":"crossref","unstructured":"Control of stress\u2010dependent cardiac growth and gene expression by a microRNA Science. 2017;316:575\u2013579.","DOI":"10.1126\/science.1139089"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(04)00045-5"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature02871"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.116.309528"},{"key":"e_1_3_2_17_2","doi-asserted-by":"publisher","DOI":"10.1007\/s00395-018-0694-x"},{"key":"e_1_3_2_18_2","first-page":"1909","article-title":"MicroRNA\u2010327 regulates\u00a0cardiac\u00a0hypertrophy and\u00a0fibrosis\u00a0induced by pressure overload","volume":"41","author":"Ji Y","year":"2018","unstructured":"Ji Y, Qiu M, Shen Y, Gao L, Wang Y, Sun W, Li X, Lu Y, Kong X. MicroRNA\u2010327 regulates\u00a0cardiac\u00a0hypertrophy and\u00a0fibrosis\u00a0induced by pressure overload. 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