{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T14:07:37Z","timestamp":1778854057097,"version":"3.51.4"},"reference-count":47,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T00:00:00Z","timestamp":1778803200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T00:00:00Z","timestamp":1778803200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["febs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FEBS Journal"],"abstract":"<jats:p>\n                    The structural and electrophysiological stability of the adult heart depends on coordinated transcriptional repression governed by chromatin remodeling and nuclear architecture. The Chd4\/NuRD complex is essential to maintain cardiomyocyte identity, and its deletion leads to arrhythmias, aberrant expression of skeletal muscle sarcomeric genes, and dysregulation of key components of the cardiac conduction system, including\n                    <jats:italic>Hcn4<\/jats:italic>\n                    ,\n                    <jats:italic>Cntn2<\/jats:italic>\n                    , and\n                    <jats:italic>Cx40<\/jats:italic>\n                    . However, while the mechanisms by which Chd4 cooperates with additional transcriptional regulators to preserve adult cardiac homeostasis remain poorly understood, previous studies have identified ThPOK, a lamina\u2010associated transcription factor, as a candidate Chd4 partner in cardiomyocytes. Using cardiomyocyte\u2010specific conditional mouse models, we show that combined loss of\n                    <jats:italic>Chd4<\/jats:italic>\n                    and\n                    <jats:italic>ThPOK<\/jats:italic>\n                    markedly exacerbates conduction defects, leading to more severe arrhythmias and accelerated sudden cardiac death compared with\n                    <jats:italic>Chd4<\/jats:italic>\n                    loss alone. Transcriptomic profiling revealed a synergistic upregulation of Sprr1a, a protein normally expressed in the epidermis where it contributes to keratinocyte differentiation and cornification.\n                    <jats:italic>Sprr1a<\/jats:italic>\n                    induction correlated with downregulation of the cardioprotective\n                    <jats:italic>microRNA miR\u2010150\u20105p<\/jats:italic>\n                    , a change driven by\n                    <jats:italic>Chd4<\/jats:italic>\n                    deletion; however,\n                    <jats:italic>miR\u2010150\u20105p<\/jats:italic>\n                    levels were not further reduced in double\u2010knockout hearts, indicating that ThPOK contributes to\n                    <jats:italic>Sprr1a<\/jats:italic>\n                    de\u2010repression through a distinct mechanism. Notably,\n                    <jats:italic>Sprr1a<\/jats:italic>\n                    upregulation was also observed in\n                    <jats:italic>Lmna<\/jats:italic>\n                    mutant hearts, suggesting a link between its de\u2010repression and cardiac\u2010specific nuclear lamina dysfunction. Together, these findings uncover a cooperative Chd4;ThPOK regulatory axis that preserves transcriptional integrity and safeguards structural and electrical homeostasis in the adult murine heart.\n                  <\/jats:p>","DOI":"10.1111\/febs.70583","type":"journal-article","created":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T13:14:51Z","timestamp":1778850891000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Chd4 and\n                    <scp>ThPOK<\/scp>\n                    cooperate to preserve structural and electrophysiological integrity of the adult heart through Sprr1a repression"],"prefix":"10.1111","author":[{"given":"Fadoua","family":"El Abdellaoui\u2010Soussi","sequence":"first","affiliation":[{"name":"Institute for Rare Diseases Research, Instituto de Salud Carlos III (ISCIII)  Madrid Spain"},{"name":"Gene Regulation in Cardiovascular Remodelling and Inflammation Laboratory Centro Nacional de Investigaciones Cardiovasculares (CNIC)  Madrid Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Apolonia","family":"Novillo","sequence":"additional","affiliation":[{"name":"Departamento de Biolog\u00eda Celular e Histolog\u00eda, Facultad de Medicina Universidad Complutense de Madrid (UCM)  Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Roc\u00edo","family":"Brea","sequence":"additional","affiliation":[{"name":"Institute for Rare Diseases Research, Instituto de Salud Carlos III (ISCIII)  Madrid Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marta","family":"Ysbert","sequence":"additional","affiliation":[{"name":"Institute for Rare Diseases Research, Instituto de Salud Carlos III (ISCIII)  Madrid Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lorena","family":"Cuss\u00f3","sequence":"additional","affiliation":[{"name":"Unidad de Imagen Avanzada Centro Nacional de Investigaciones 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Luis","family":"Armesilla","sequence":"additional","affiliation":[{"name":"Centro de Investigaci\u00f3n Biom\u00e9dica en Red de Enfermedades Cardiovasculares (CIBERCV)  Madrid Spain"},{"name":"Facultad HM de Ciencias de la Salud Universidad Camilo Jos\u00e9 Cela  Madrid Spain"},{"name":"Instituto de Investigaci\u00f3n Sanitaria HM Hospitales  Madrid Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8822-8274","authenticated-orcid":false,"given":"Ignacio","family":"P\u00e9rez de Castro","sequence":"additional","affiliation":[{"name":"Institute for Rare Diseases Research, Instituto de Salud Carlos III (ISCIII)  Madrid Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alicia R.","family":"Folgueras","sequence":"additional","affiliation":[{"name":"Departamento de Bioqu\u00edmica y Biolog\u00eda Molecular, Facultad de Medicina Instituto Universitario de Oncolog\u00eda del Principado de Asturias (IUOPA), Universidad de 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