Eduardo N. Chini

This study identifies succinate accumulation in aged ovarian tumor microenvironments as a driver of Treg dysfunction, suggesting metabolic targeting as a strategy to restore antitumor immunity.

This study shows that loss of LATS1/2 in endothelial cells promotes a senescence-associated stemness (SAS) state, leading to atherothrombotic plaque formation through metabolic and mitochondrial dysregulation.

This study shows that CD38 in astrocytes mediates NAD+ depletion and myelin damage caused by high fat diets and demyelination, with CD38 inhibitors improving myelin regeneration.