My research focuses in identify targetable mechanisms and pathways underlying initiation and progression of diabetic complications with potential therapeutic value.

In have investigated and successfully published a study in which we looked at whether the calcium-calcineurin transcription factor NFAT was involved in diabetic-driven endothelial and kidney dysfunction in the novel Akita mouse model of diabetes type 1.  

The project that I am working at the moment focuses on exploring if the blockade of diabetes induced NFAT activation in the heart of the Akita mouse model exerts cardioprotective effects against the development of diabetic cardiomyopathy.