{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,1]],"date-time":"2026-06-01T23:54:15Z","timestamp":1780358055495,"version":"3.54.1"},"reference-count":56,"publisher":"SAGE Publications","issue":"6","license":[{"start":{"date-parts":[[2024,6,1]],"date-time":"2024-06-01T00:00:00Z","timestamp":1717200000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Thyroid\u00ae"],"published-print":{"date-parts":[[2024,6]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Thyroid hormones regulate cardiac functions mainly through direct actions in the heart and by binding to the thyroid hormone receptor (TR) isoforms \u03b11 and \u03b2. While the role of the most abundantly expressed isoform, TR\u03b11, is widely studied and well characterized, the role of TR\u03b2 in regulating heart functions is still poorly understood, primarily due to the accompanying elevation of circulating thyroid hormone in TR\u03b2 knockout mice (TR\u03b2-KO). However, their hyperthyroidism is ameliorated at thermoneutrality, which allows studying the role of TR\u03b2 without this confounding factor.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>Here, we noninvasively monitored heart rate in TR\u03b2-KO mice over several days using radiotelemetry at different housing temperatures (22\u00b0C and 30\u00b0C) and upon 3,3\u2032,5-triiodothyronine (T3) administration in comparison to wild-type animals.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      TR\u03b2-KO mice displayed normal average heart rate at both 22\u00b0C and 30\u00b0C with only minor changes in heart rate frequency distribution, which was confirmed by independent electrocardiogram recordings in freely-moving conscious mice. Parasympathetic nerve activity was, however, impaired in TR\u03b2-KO mice at 22\u00b0C, and only partly rescued at 30\u00b0C. As expected, oral treatment with pharmacological doses of T3 at 30\u00b0C led to tachycardia in wild-types, accompanied by broader heart rate frequency distribution and increased heart weight. The TR\u03b2-KO mice, in contrast, showed blunted tachycardia, as well as resistance to changes in heart rate frequency distribution and heart weight. At the molecular level, these observations were paralleled by a blunted cardiac mRNA induction of several important genes, including the pacemaker channels\n                      <jats:italic toggle=\"yes\">Hcn2<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">Hcn4<\/jats:italic>\n                      , as well as\n                      <jats:italic toggle=\"yes\">Kcna7<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>The phenotyping of TR\u03b2-KO mice conducted at thermoneutrality allows novel insights on the role of TR\u03b2 in cardiac functions in the absence of the usual confounding hyperthyroidism. Even though TR\u03b2 is expressed at lower levels than TR\u03b11 in the heart, our findings demonstrate an important role for this isoform in the cardiac response to thyroid hormones.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1089\/thy.2023.0638","type":"journal-article","created":{"date-parts":[[2024,3,25]],"date-time":"2024-03-25T10:35:28Z","timestamp":1711362928000},"page":"796-805","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":5,"title":["Partial Resistance to Thyroid Hormone\u2013Induced Tachycardia and Cardiac Hypertrophy in Mice Lacking Thyroid Hormone Receptor \u03b2"],"prefix":"10.1177","volume":"34","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5988-9885","authenticated-orcid":false,"given":"Riccardo","family":"Dore","sequence":"first","affiliation":[{"name":"Institute for Experimental Endocrinology, Center of Brain Behavior &amp; Metabolism, University of L\u00fcbeck, L\u00fcbeck, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah Christine","family":"Sentis","sequence":"additional","affiliation":[{"name":"Institute for Experimental Endocrinology, Center of Brain Behavior &amp; Metabolism, University of L\u00fcbeck, L\u00fcbeck, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5089-7237","authenticated-orcid":false,"given":"Kornelia","family":"Johann","sequence":"additional","affiliation":[{"name":"Institute for Experimental Endocrinology, Center of Brain Behavior &amp; Metabolism, University of L\u00fcbeck, L\u00fcbeck, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nuria","family":"Lopez-Alcantara","sequence":"additional","affiliation":[{"name":"Institute for Experimental Endocrinology, Center of Brain Behavior &amp; Metabolism, University of L\u00fcbeck, L\u00fcbeck, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julia","family":"Resch","sequence":"additional","affiliation":[{"name":"Institute for Experimental Endocrinology, Center of Brain Behavior &amp; Metabolism, University of L\u00fcbeck, L\u00fcbeck, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akila","family":"Chandrasekar","sequence":"additional","affiliation":[{"name":"Institute for Experimental and Clinical Pharmacology and Toxicology, Center of Brain Behavior &amp; Metabolism, University of L\u00fcbeck, L\u00fcbeck, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2815-4426","authenticated-orcid":false,"given":"Helge","family":"M\u00fcller-Fielitz","sequence":"additional","affiliation":[{"name":"Institute for Experimental and Clinical Pharmacology and Toxicology, Center of Brain Behavior &amp; Metabolism, University of L\u00fcbeck, L\u00fcbeck, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lars Christian","family":"Moeller","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Diabetes and Metabolism, and Division of Laboratory Research, University of Duisburg-Essen, Essen, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dagmar","family":"Fuehrer","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Diabetes and Metabolism, and Division of Laboratory Research, University of Duisburg-Essen, Essen, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Markus","family":"Schwaninger","sequence":"additional","affiliation":[{"name":"Institute for Experimental and Clinical Pharmacology and Toxicology, Center of Brain Behavior &amp; Metabolism, University of L\u00fcbeck, L\u00fcbeck, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benedikt","family":"Obermayer","sequence":"additional","affiliation":[{"name":"Core Unit Bioinformatics, Berlin Institute of Health at Charit\u00e9, Universit\u00e4tsmedizin Berlin, Berlin, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"Opitz","sequence":"additional","affiliation":[{"name":"Institute of Experimental Pediatric Endocrinology, Charit\u00e9 Universit\u00e4tsmedizin Berlin, Berlin, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7778-5158","authenticated-orcid":false,"given":"Jens","family":"Mittag","sequence":"additional","affiliation":[{"name":"Institute for Experimental Endocrinology, Center of Brain Behavior &amp; Metabolism, University of L\u00fcbeck, L\u00fcbeck, 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