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The mutation of collagen VI can result in Ullrich congenital muscular dystrophy and Bethlem myopathy, pointing to a critical function in muscle physiology. However, the functional role of collagen VI in the heart is poorly understood. In human heart failure with reduced ejection fraction, collagen VI is increased within the remodeled T\u2010tubules, suggesting a possible role in tubular structure and Ca\n                      <jats:sup>2+<\/jats:sup>\n                      dynamics.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      To investigate this hypothesis, a global knockout of the collagen VI alpha 1 gene (Col6a1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      ) was generated in the rat.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      T\u2010tubule structure and ryanodine receptor cluster organization were unchanged, but echocardiography demonstrated reduced systolic function. Consistent with this, isolated trabeculae from Col6a1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      hearts generated significantly less peak stress, confirming impaired contractile force at the tissue level. Paradoxically, isolated cardiomyocytes from the Col6a1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      rat had increased Ca\n                      <jats:sup>2+<\/jats:sup>\n                      transient amplitude and increased sarcoplasmic reticulum Ca\n                      <jats:sup>2+<\/jats:sup>\n                      load that would be expected to increase force. \u03b2\u2010adrenergic stimulation further increased Ca\n                      <jats:sup>2+<\/jats:sup>\n                      transient amplitude and was associated with diastolic Ca\n                      <jats:sup>2+<\/jats:sup>\n                      release events in Col6a1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      cardiomyocytes. Furthermore, \u03b2\u2010adrenergic stimulation of Col6a1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      trabeculae exhibited spontaneous contractions, indicating an increased susceptibility to arrhythmic activity.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Together, these results indicate collagen VI has a role in both force transduction and Ca\n                      <jats:sup>2+<\/jats:sup>\n                      cycling in the heart.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/apha.70144","type":"journal-article","created":{"date-parts":[[2025,12,22]],"date-time":"2025-12-22T09:56:13Z","timestamp":1766397373000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["The Absence of Collagen VI Reduces Systolic Function but Paradoxically Increases Ca\n                    <sup>2+<\/sup>\n                    Release in the Rat Heart"],"prefix":"10.1111","volume":"242","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2072-5290","authenticated-orcid":false,"given":"A.","family":"Krstic","sequence":"first","affiliation":[{"name":"Department of Physiology, School of Medical and Health Sciences, Faculty of Medical and Health Sciences, Manaaki Manawa\u2014The Centre for Heart Research Waipapa Taumata Rau\/The University of Auckland  Auckland New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H.","family":"Moammer","sequence":"additional","affiliation":[{"name":"Department of Physiology, School of Medical and Health Sciences, Faculty of Medical and Health Sciences, Manaaki Manawa\u2014The Centre for Heart Research Waipapa Taumata Rau\/The University of Auckland  Auckland New Zealand"},{"name":"Department of Clinical Physiology, Faculty of Medicine King Abdulaziz University  Jeddah Saudi Arabia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6185-9906","authenticated-orcid":false,"given":"S.","family":"Hassan","sequence":"additional","affiliation":[{"name":"Department of Physiology, School of Medical and Health Sciences, Faculty of Medical and Health Sciences, Manaaki Manawa\u2014The Centre for Heart Research Waipapa Taumata Rau\/The University of Auckland  Auckland New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Bai","sequence":"additional","affiliation":[{"name":"Department of Physiology, School of Medical and Health Sciences, Faculty of Medical and Health Sciences, Manaaki Manawa\u2014The Centre for Heart Research Waipapa Taumata Rau\/The University of Auckland  Auckland New 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