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<p>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 <i>in viv</i>o 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.</p>

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TRPV1 deletion in male mice alters cardiomyocyte ultrastructure without affecting baseline cardiac function

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月21日

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  • Nolwenn Tessier,
  • Lucille Païta,
  • Christophe Chouabe,
  • Hélène Thibault,
  • Margaux Melka,
  • Mallory Ducrozet,
  • Ribal Al-Mawla,
  • Rania Harisseh,
  • Christelle Léon,
  • Lionel Augeul,
  • Sylvie Dupré-Aucouturier,
  • Gabriel Bidaux,
  • Michel Ovize,
  • Fabien Van Coppenolle,
  • Sylvie Ducreux

摘要

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.