TRPV1 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.