biostudies-literatureTessier NAgence Nationale de la RechercheInstitut National de la Santé et de la Recherche Médicale45781https://www.ebi.ac.uk/biostudies/studies/S-EPMC12756331biostudies-literatureUnknown15(1)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^⁻/⁻) and wild-type (TRPV1^⁺/⁺) 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^-/- 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.Scientific reportsTRPV1 deletion in male mice alters cardiomyocyte ultrastructure without affecting baseline cardiac function.PMC12756331132484/BR/VO-Réf INSERM: 131589A10ANR-10-IBHU-004Sylvie DABidaux GPaita LLeon CMelka MHarisseh ROvize MDucrozet MVan Coppenolle FDucreux SAl-Mawla RAugeul LThibault HChouabe CTessier NfalseTRPV1 deletion in male mice alters cardiomyocyte ultrastructure without affecting baseline cardiac function.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^⁻/⁻) and wild-type (TRPV1^⁺/⁺) 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^-/- 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.2025-01-01T00:00:00Z2025 Dec2026-06-25T03:23:47.689Z2026-06-25T03:08:24.518ZS-EPMC127563314142346610.1038/s41598-025-28521-5