A combined preclinical, human genetics, and patient-data study reported that SGLT2 inhibitors can protect coronary microvessels by preserving the endothelial glycocalyx during ischemia-reperfusion injury. The work ties vascular function improvements to a specific protective mechanism—glycocalyx degradation prevention—rather than broader inflammatory endpoints alone. The finding may strengthen mechanistic support for SGLT2 inhibitor use in patients at cardiovascular risk, especially where microvascular dysfunction contributes to persistent symptoms or adverse outcomes. For drug developers and clinicians, the next practical question is whether the glycocalyx-preservation effect can be measured reliably in humans and whether it maps to clinical events in dedicated trials.