{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tessier N"],"funding":["Agence Nationale de la Recherche","Institut National de la Santé et de la Recherche Médicale"],"pagination":["45781"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12756331"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_abstract":["The Transient Receptor Potential Vanilloid 1 (TRPV1) channel is implicated in various cardiovascular processes, including nociception, inflammation, and ischemia-reperfusion injury, yet its role in maintaining baseline cardiac structure and function remains unclear. To address this, we performed a bibliometric analysis of 331 publications (2004-2025) and conducted in vivo and ex vivo cardiac phenotyping of sedentary male TRPV1 knockout (TRPV1<sup>⁻/⁻</sup>) and wild-type (TRPV1<sup>⁺/⁺</sup>) mice (8-16 weeks). Echocardiography, patch-clamp electrophysiology, Ca²⁺ handling assays, mitochondrial function tests, and ultrastructural analyses were employed. Bibliometric mapping identified three major research clusters related to TRPV1 in cardiovascular science: ischemia-reperfusion injury, vascular/metabolic regulation, and autonomic control, with no prior studies assessing baseline cardiac function in TRPV1<sup>-/-</sup> mice. Functional assessments revealed no significant differences between genotypes in echocardiographic parameters, action potential properties, L-type Ca²⁺ currents, Na⁺-Ca²⁺ exchange, or mitochondrial performance. Ca²⁺ 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."],"journal":["Scientific reports"],"pubmed_title":["TRPV1 deletion in male mice alters cardiomyocyte ultrastructure without affecting baseline cardiac function."],"pmcid":["PMC12756331"],"funding_grant_id":["132484/BR/VO-Réf INSERM: 131589A10","ANR-10-IBHU-004"],"pubmed_authors":["Sylvie DA","Bidaux G","Paita L","Leon C","Melka M","Harisseh R","Ovize M","Ducrozet M","Van Coppenolle F","Ducreux S","Al-Mawla R","Augeul L","Thibault H","Chouabe C","Tessier N"],"additional_accession":[]},"is_claimable":false,"name":"TRPV1 deletion in male mice alters cardiomyocyte ultrastructure without affecting baseline cardiac function.","description":"The Transient Receptor Potential Vanilloid 1 (TRPV1) channel is implicated in various cardiovascular processes, including nociception, inflammation, and ischemia-reperfusion injury, yet its role in maintaining baseline cardiac structure and function remains unclear. To address this, we performed a bibliometric analysis of 331 publications (2004-2025) and conducted in vivo and ex vivo cardiac phenotyping of sedentary male TRPV1 knockout (TRPV1<sup>⁻/⁻</sup>) and wild-type (TRPV1<sup>⁺/⁺</sup>) mice (8-16 weeks). Echocardiography, patch-clamp electrophysiology, Ca²⁺ handling assays, mitochondrial function tests, and ultrastructural analyses were employed. Bibliometric mapping identified three major research clusters related to TRPV1 in cardiovascular science: ischemia-reperfusion injury, vascular/metabolic regulation, and autonomic control, with no prior studies assessing baseline cardiac function in TRPV1<sup>-/-</sup> mice. Functional assessments revealed no significant differences between genotypes in echocardiographic parameters, action potential properties, L-type Ca²⁺ currents, Na⁺-Ca²⁺ exchange, or mitochondrial performance. Ca²⁺ 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.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Dec","modification":"2026-06-25T03:23:47.689Z","creation":"2026-06-25T03:08:24.518Z"},"accession":"S-EPMC12756331","cross_references":{"pubmed":["41423466"],"doi":["10.1038/s41598-025-28521-5"]}}