{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T12:59:53Z","timestamp":1790341193084,"version":"4.1.0"},"reference-count":36,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T00:00:00Z","timestamp":1786060800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T00:00:00Z","timestamp":1786060800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Proteomics Clinical Apps"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Purpose<\/jats:title>\n                    <jats:p>In heart failure, dyssynchrony is associated with accelerated cardiac remodeling and a worse prognosis. Both restored with resynchronization. We have previously developed a mouse model of dyssynchrony and resynchronization and here assess changes in protein expression within that model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental design<\/jats:title>\n                    <jats:p>Mice were subjected to ischemia\/reperfusion followed by pacemaker implantation. Three groups were defined: (i) sinus rhythm for 4\u00a0weeks\u2014synchronous heart failure (SynHF), (ii) right ventricular pacing (RVP) for 4\u00a0weeks\u2014dyssynchronous heart failure (DysHF), and (iii) RVP for 2\u00a0weeks followed by 2\u00a0weeks of sinus rhythm\u2014resynchronized heart failure (ResynHF). Heart tissue was evaluated for protein content with mass spectrometry.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>A total of 3324 proteins were detected. The abundance of 589 proteins differed between DysHF and SynHF and 253 between DysHF and ResynHF. The changed proteins in the comparisons to DysHF overlapped to a great extent. Several of these proteins were connected to calcium handling or made up part of the sarcomere.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Adding dyssynchrony to ischemic heart failure resulted in protein dysregulation, which was partly reversed by resynchronization. The dysregulation was characterized by a change in proteins related to contractility, which may be part of the positive inotropic effect and reverse remodeling observed with resynchronization.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/prca.70052","type":"journal-article","created":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T11:49:48Z","timestamp":1786103388000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Proteomic Remodeling in the Failing Left Ventricle Adapting to Dyssynchrony"],"prefix":"10.1002","volume":"20","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-0787-9254","authenticated-orcid":false,"given":"Karin","family":"Ljung","sequence":"first","affiliation":[{"name":"Department of Medicine Karolinska Institutet and ME Cardiology Heart and Vascular Centre Karolinska University Hospital  Solna Stockholm Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nitha Aima","family":"Muntu","sequence":"additional","affiliation":[{"name":"Department of Cell and Molecular Physiology Loyola University Chicago Stritch School of Medicine  Chicago Illinois USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9192-8992","authenticated-orcid":false,"given":"Ulrika","family":"Reistam","sequence":"additional","affiliation":[{"name":"Department of Medicine Karolinska Institutet and ME Cardiology Heart and Vascular Centre Karolinska University Hospital  Solna Stockholm Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5192-2860","authenticated-orcid":false,"given":"Jonathan A.","family":"Kirk","sequence":"additional","affiliation":[{"name":"Department of Cell and Molecular Physiology Loyola University Chicago Stritch School of Medicine  Chicago Illinois USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0319-6240","authenticated-orcid":false,"given":"Marcus","family":"St\u00e5hlberg","sequence":"additional","affiliation":[{"name":"Department of Medicine Karolinska Institutet and ME Cardiology Heart and Vascular Centre Karolinska University Hospital  Solna Stockholm Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,8,7]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.1093\/europace\/euy035"},{"key":"e_1_2_10_3_1","doi-asserted-by":"crossref","unstructured":"J. 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