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To address this, we performed a bibliometric analysis of 331 publications (2004\u20132025) and conducted\n                    <jats:italic>in viv<\/jats:italic>\n                    o and ex vivo cardiac phenotyping of sedentary male TRPV1 knockout (TRPV1\n                    <jats:sup>\u207b\/\u207b<\/jats:sup>\n                    ) and wild-type (TRPV1\n                    <jats:sup>\u207a\/\u207a<\/jats:sup>\n                    ) mice (8\u201316 weeks). Echocardiography, patch-clamp electrophysiology, Ca\u00b2\u207a handling assays, mitochondrial function tests, and ultrastructural analyses were employed. Bibliometric mapping identified three major research clusters related to TRPV1 in cardiovascular science: ischemia\u2013reperfusion injury, vascular\/metabolic regulation, and autonomic control, with no prior studies assessing baseline cardiac function in TRPV1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. Functional assessments revealed no significant differences between genotypes in echocardiographic parameters, action potential properties, L-type Ca\u00b2\u207a currents, Na\u207a\u2013Ca\u00b2\u207a exchange, or mitochondrial performance. Ca\u00b2\u207a transient kinetics exhibited minor alterations without functional impact. Ultrastructural evaluation revealed subtle changes, including slightly longer sarcomeres and altered nuclear morphology (reduced circularity and solidity), while reticulum-mitochondria interfaces remained intact. These findings indicate that deleting TRPV1 does not substantially impair basic cardiac function in young male mice, suggesting a limited role in normal physiology and potential relevance primarily under pathological or stress-induced conditions.\n                  <\/jats:p>","DOI":"10.1038\/s41598-025-28521-5","type":"journal-article","created":{"date-parts":[[2025,12,21]],"date-time":"2025-12-21T16:04:23Z","timestamp":1766333063000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["TRPV1 deletion in male mice alters cardiomyocyte ultrastructure without affecting baseline cardiac function"],"prefix":"10.1038","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2132-8489","authenticated-orcid":false,"given":"Nolwenn","family":"Tessier","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lucille","family":"Pa\u00efta","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1517-1438","authenticated-orcid":false,"given":"Christophe","family":"Chouabe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9784-0425","authenticated-orcid":false,"given":"H\u00e9l\u00e8ne","family":"Thibault","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Margaux","family":"Melka","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mallory","family":"Ducrozet","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0734-985X","authenticated-orcid":false,"given":"Ribal","family":"Al-Mawla","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rania","family":"Harisseh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8229-5401","authenticated-orcid":false,"given":"Christelle","family":"L\u00e9on","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2832-8089","authenticated-orcid":false,"given":"Lionel","family":"Augeul","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sylvie","family":"Dupr\u00e9-Aucouturier","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6162-3223","authenticated-orcid":false,"given":"Gabriel","family":"Bidaux","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michel","family":"Ovize","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1682-8959","authenticated-orcid":false,"given":"Fabien","family":"Van Coppenolle","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3207-9537","authenticated-orcid":false,"given":"Sylvie","family":"Ducreux","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,12,21]]},"reference":[{"key":"28521_CR1","doi-asserted-by":"publisher","first-page":"11","DOI":"10.1007\/s00424-005-1429-z","volume":"451","author":"BN Desai","year":"2005","unstructured":"Desai, B. N. & Clapham, D. E. TRP channels and mice deficient in TRP channels. Pflugers Arch. 451, 11\u201318 (2005).","journal-title":"Pflugers Arch."},{"key":"28521_CR2","doi-asserted-by":"publisher","first-page":"816","DOI":"10.1038\/39807","volume":"389","author":"MJ Caterina","year":"1997","unstructured":"Caterina, M. J. et al. The capsaicin receptor: a heat-activated ion channel in the pain pathway. Nature 389, 816\u2013824 (1997).","journal-title":"Nature"},{"key":"28521_CR3","doi-asserted-by":"publisher","first-page":"517","DOI":"10.1038\/nature02196","volume":"426","author":"DE Clapham","year":"2003","unstructured":"Clapham, D. E. TRP channels as cellular sensors. Nature 426, 517\u2013524 (2003).","journal-title":"Nature"},{"key":"28521_CR4","doi-asserted-by":"publisher","first-page":"306","DOI":"10.1126\/science.288.5464.306","volume":"288","author":"MJ Caterina","year":"2000","unstructured":"Caterina, M. J. et al. 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