TRPV1 Deletion in Male Mice Alters Cardiomyocyte Ultrastructure Without Affecting Baseline Cardiac Function

Abstract BackgroundThe Transient Receptor Potential Vanilloid 1 (TRPV1) channel has been implicated in various cardiovascular processes, including nociception, inflammation, and ischemia-reperfusion injury. However, its role in maintaining baseline cardiac structure and function remains unclear.ObjectivesTo investigate whether TRPV1 deletion affects cardiac function and ultrastructure under physiological conditions and to identify research trends related to TRPV1 in cardiovascular science.MethodsWe combined a bibliometric analysis of 331 publications (2004–2025) on TRPV1 and cardiovascular health with in vivo and ex vivo phenotyping of TRPV1 knockout (TRPV1⁻/⁻) and wild-type (TRPV1⁺/⁺) male mice. Echocardiography, patch-clamp electrophysiology, Ca²⁺ handling assays, mitochondrial function tests, and ultrastructural analyses were performed.ResultsBibliometric mapping revealed three major research clusters: TRPV1 in ischemia–reperfusion injury, vascular/metabolic regulation, and autonomic control, but no prior studies assessed baseline cardiac function in TRPV1⁻/⁻ mice. Our functional analyses showed 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.ConclusionDeleting TRPV1 does not impair basic heart function but causes minor structural changes. This indicates a limited role in normal physiology and possible relevance only in pathological conditions.