Endothelial dysfunction has traditionally been defined by impaired nitric oxide-dependent vasodilation, following the classical Furchgott paradigm. However, growing evidence indicates that other autacoids, including prostacyclin, hydrogen sulphide, and angiotensin-(1-7), interact with nitric oxide signalling, and that the integrity of the endothelial glycocalyx is an increasingly important determinant of vascular health. A major area of uncertainty concerns the relationship between endothelial vasomotor function and glycocalyx integrity: these often co-occur in conditions such as pulmonary hypertension and diabetes, yet whether one is primary and the other secondary, or whether they arise through independent mechanisms, remains unclear. This distinction matters because it is not known whether correcting one component of endothelial dysfunction would improve the others. Beidong's research aims to address this uncertainty, with a view to informing how endothelial dysfunction is characterised and how future therapeutic strategies might be designed.