Cardiac fibroblast (CF) activation in response to injury or inflammation is a central driver of pathological cardiac fibrosis, contributing to arrhythmias and heart failure. As previously demonstrated, intermittent hypoxia (IH), the hallmark pathophysiological feature of obstructive sleep apnoea (OSA), induces cardiac fibrosis. However, the mechanisms by which IH promotes CF activation and the key molecular mediators involved remain unclear.