{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T13:11:59Z","timestamp":1789564319833,"version":"build-2803163510"},"reference-count":39,"publisher":"Wiley","issue":"20","license":[{"start":{"date-parts":[[2024,10,16]],"date-time":"2024-10-16T00:00:00Z","timestamp":1729036800000},"content-version":"vor","delay-in-days":15,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2024,10,1]],"date-time":"2024-10-01T00:00:00Z","timestamp":1727740800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Physiological Reports"],"published-print":{"date-parts":[[2024,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Correlation between echocardiographic and pathoanatomic variables and their prognostic value in murine cardiomyopathy models remain unknown. Using echocardiography, morphometrics, and survival monitoring, we characterized transgenic (TG) mice with dilated cardiomyopathy due to cardiac overexpression of \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    \u2010adrenoceptors focusing on predicting heart failure (HF) risk and HF mortality. In 12\u2010month\u2010old non\u2010TG and TG mice, echocardiography was performed to determine left ventricular (LV) dimensions (d), wall thickness (h), and fractional shortening (FS). Animals were monitored for 3\u2009months for survival. Organ weights and pathological events indicating left HF were determined. TG mice (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u200976) had reduced FS and enlarged LV, and 79% died of HF or likely arrhythmias during the follow\u2010up period while all non\u2010TG mice (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u200926) survived. These mice with left HF also had pulmonary congestion and hypertrophy\/dilatation of the right ventricle (RV). Weights of lungs, RV, and atria were intercorrelated (\n                    <jats:italic>r<\/jats:italic>\n                    \u2009=\u20090.79\u20130.83) and also negatively correlated with FS\u2009\u00d7\u2009(\n                    <jats:italic>h<\/jats:italic>\n                    \/\n                    <jats:italic>d<\/jats:italic>\n                    ) index (\n                    <jats:italic>r<\/jats:italic>\n                    \u2009=\u2009\u22120.502 to \u22120.609). By FS\u2009\u00d7\u2009(\n                    <jats:italic>h<\/jats:italic>\n                    \/\n                    <jats:italic>d<\/jats:italic>\n                    ) tertiles, TG mice of low tertiles were identified with the highest mortality (96%) largely due to HF (76%). In conclusion, in aged cardiomyopathy mice a good correlation existed between echocardiographic and pathoanatomic variables. Echocardiography\u2010derived LV function and remodeling were useful in identifying a subgroup of TG mice with a high risk of HF and HF fatality.\n                  <\/jats:p>","DOI":"10.14814\/phy2.70061","type":"journal-article","created":{"date-parts":[[2024,10,16]],"date-time":"2024-10-16T04:25:03Z","timestamp":1729052703000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["EXPRESSION OF CONCERN: Cardiomyopathy characterizing and heart failure risk predicting by echocardiography and pathoanatomy in aged male mice"],"prefix":"10.14814","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5213-3911","authenticated-orcid":false,"given":"Xiao\u2010Jun","family":"Du","sequence":"first","affiliation":[{"name":"Department of Physiology and Pathophysiology, School of Basic Medical Sciences Xi'an Jiaotong University Health Science Center  Xi'an Shaanxi China"},{"name":"Experimental Cardiology Baker Heart and Diabetes Institute  Melbourne Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin\u2010Heng","family":"Feng","sequence":"additional","affiliation":[{"name":"Experimental Cardiology Baker Heart and Diabetes Institute  Melbourne Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zi\u2010Qiu","family":"Ming","sequence":"additional","affiliation":[{"name":"Experimental Cardiology Baker Heart and Diabetes Institute  Melbourne Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helen","family":"Kiriazis","sequence":"additional","affiliation":[{"name":"Experimental Cardiology Baker Heart and Diabetes Institute  Melbourne Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2024,10,16]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.1097\/00019501-200502000-00002"},{"key":"e_1_2_10_3_1","doi-asserted-by":"publisher","DOI":"10.1136\/heartjnl-2019-315942"},{"key":"e_1_2_10_4_1","doi-asserted-by":"publisher","DOI":"10.1093\/ehjci\/jey065"},{"key":"e_1_2_10_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2023.05.064"},{"key":"e_1_2_10_6_1","doi-asserted-by":"publisher","DOI":"10.1152\/physiolgenomics.00005.2003"},{"key":"e_1_2_10_7_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.11.6400"},{"key":"e_1_2_10_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(01)00244-9"},{"key":"e_1_2_10_9_1","first-page":"47","article-title":"Sympatho\u2010adrenergic mechanisms in heart failure: New insights into pathophysiology","volume":"1","author":"Du X. 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