The heart is a complex organ composed of multiple cell types working together to maintain its rhythmic and contractile function. Among the key cell types within the heart are myocytes and cardiac fibroblasts. Myocytes are the primary muscle cells responsible for the mechanical contraction of the heart, enabling it to pump blood efficiently throughout the body. Fibroblasts are the most abundant non-myocyte cells in the heart, and they are responsible for producing and maintaining the extracellular matrix, which provides structural and mechanical support for the cardiac tissue. Fibroblasts number further increases with ageing and pathological conditions [1]. Traditionally considered as passive cells providing structural support, research has now unveiled an active and dynamic role for cardiac fibroblasts in modulating cardiac electrophysiology. In addition to forming passive obstacles to electrical conduction, fibroblasts have been proposed to actively affect cardiac conduction, myocyte excitability, contractility, action potential duration and calcium cycling. Mechanisms include heterocellular cell-cell coupling and paracrine communication [2]. Functional fibroblast-myocyte coupling mediated by gap junctions or tunnelling nanotubes has been observed both in vitro and in situ in animal models [3,4,5]. Importantly, in situ this coupling is limited to cells in the sinoatrial node and in the ventricle at the border zone of post-myocardial infarcts [5,6]. Coupling also occurs between senescence fibroblasts and myocytes at the infarct border zone in the aged rabbit heart, promoting significant arrhythmogenic remodelling [7]. Paracrine communication, mediated by cytokines and growth factors released by cardiac fibroblasts, has also been shown to influence myocyte electrophysiology and calcium handling in animal cell cultures [8,9]. Recently, advanced human cell coculture systems mimicking different cell-cell interaction modalities have been employed to assess the contribution of contact versus paracrine interactions. Activated human cardiac fibroblasts exert adverse effects on the electrophysiological and Ca²⁺ handling of human myocytes and downregulate voltage channels (K_V4.3, K_V11.1 and Kir6.2) and SERCA2a calcium pump. Interleukin-6 and connexin43 were identified as paracrine- and contact-mediators driving these effects [10]. Thus, fibroblast-myocyte interactions are complex and dynamic processes that play a crucial role in cardiac electrophysiology. Understanding these interactions can help to elucidate the mechanisms of normal and abnormal cardiac function, as well as to develop novel strategies for preventing and treating cardiac arrhythmias and progression to heart failure. Details of fibroblast-myocyte interactions in disease conditions such as ischemia-reperfusion injury, hypertrophic and dilated cardiomyopathy as well as in the ageing heart are still poorly explored and form a potentially exciting target for further research. Emerging tools and experimental model systems [11,12] will be invaluable to accelerate this research.