Luciana Mateus Gonçalves

This study shows hIAPP aggregation disrupts islet microvascular stability by downregulating EC genes and causing pericyte detachment, impairing vasomotor responses.

This paper identifies post-inhibitory rebound (PIR) in pancreatic islets as a mechanism converting δ-cell inhibition into excitation, revealing dynamic paracrine signaling rather than static inhibition.

This study shows that pericyte dysfunction in pancreatic islets leads to vascular abnormalities and inflammation before diabetes onset in mice treated with streptozotocin.