In type 1 diabetes, the heart develops fibrosis and vascular damage that contribute to the heart’s eventual failure. Substance P, a molecule that activates the neurokinin-1 receptor, is reduced in diabetes, predisposing the heart to these adverse changes.
The current proposal will explore interactions between substance P, the neurokinin 1 receptor, and adverse changes in the type 1 diabetic heart to assess the potential of activating the neurokinin 1 receptor as a therapy for adverse changes in the type 1 diabetic heart.