Understanding the pathological role of neuropeptide Y in myocardial ischemia-reperfusion

When a heart attack occurs, a blockage in one of the coronary arteries deprives a portion of the heart of oxygen and nutrients. To address this, reperfusion therapy is regularly administered to patients experiencing acute myocardial infarction, restoring blood flow to the heart. While this treatment is cardioprotective in the long run, the process of infarction followed by reperfusion is known to be associated with arrhythmias and structural damage to the heart. To mitigate or prevent such damage, it is crucial to deepen our understanding of its underlying mechanisms, which constitutes the primary objective of this project.

Our focus will be specifically on Neuropeptide Y, a sympathetic co-transmitter released during myocardial infarction, which contributes to reperfusion-induced damage. Employing a combination of imaging techniques and computer modeling, we aim to unravel the intricate interplay between disruptions in cellular calcium handling and the activation of a range of signaling pathways following Neuropeptide Y release. Through this investigation, we seek to elucidate how these factors may promote reperfusion-induced arrhythmias and lead to long-term adverse remodeling of the heart.