Neda’s research interest is involving the development of a fundamental understanding of key contributors to cardiac energetics that provide a comprehensive understanding of human heart disease. The research work broadly looks into the important role of mitochondrial dysfunction in the heart failure, using High Capacity Runner (HCR) and Low Capacity Runner (LCR) animal model system. Mainly focusing on the role of calcium mediating cardiac TCA cycle dehydrogenase using fatty acids, and investigating the impact of substrates such as pyruvate and fatty acid selection on the maximal velocity (Vmax) and metabolic/energetic dysfunction of the heart.
She has observed that:
- The LCR model have markedly lower fatty acid oxidation capacity than the HCR model.
- The LCR model showed no difference from HCR model in terms of cardiac function (stroke volume, EF, etc.), or ATP synthesis capacity using carbohydrate substrate.
- The HCR model have shown extra high metabolic capacity for fatty acids.
Differences in ejection fraction, phosphate levels, oxidative capacity for two different substrates (palmitoyl-L-carnitine/malate and pyruvate/malate), total adenine nucleotide and creatine between LCR and HCR rats.