|Education||MS, Universtiy of Newcastle Upon Tyne|
Heart failure affects about 5.1 million people in United States. A limited number of effective therapies are available, but these only provide symptomatic relief. As a multifactorial complex disease with many genes, proteins and metabolites being altered, heart failure requires targeted subtler approaches. In this context, our lab, and others, have found a growing body of evidence in the past decade implicating mitochondrial deterioration as a contributing factor to heart failure (HF). My approach is to explore, and selectively modify, using emerging DNA- targeting technologies, key upstream or downstream control points in the pathways that regulate mitochondrial biogenesis and quality control to develop novel future therapies for heart failure. I am specifically targeting cAMP response element sequences located upstream of mitochondrial biogenesis genes such as PPARGC1a to help kick-start the mitochondrial biogenesis pathway in failing hearts.