Howard Young

Biography

Howard Young is a professor belongs to the department of Biochemistry from the university of Alberta.

Research Interest

Inside heart cells, changes in calcium metabolism control the rate and force of muscle contraction and relaxation. With each heart beat, calcium is released from a storage compartment (the ‘sarcoplasmic reticulum’) for muscle contraction and pumped back into the storage compartment for muscle relaxation. Defects in this process are known to be associated with heart failure, and hereditary forms of heart disease may be more common than originally thought. Recently, families suffering from inherited heart disease have been found to have defects at a particular step in calcium metabolism (in proteins called ‘phospholamban’ and ‘sarcolipin’). These defects interfere with the ability of the heart to respond to changes in calcium metabolism, yet we do not fully understand the reason the genetic defects cause heart failure. The premise of our research is that the development of treatments for heart disease requires detailed knowledge of the underlying disease-associated mechanisms. Given the link between phospholamban, sarcolipin and heart failure, a detailed understanding should lead to clinical improvement in patients suffering from heart disease. Our research focuses on detecting new mutations in heart failure patients and understanding the associated molecular defects in calcium metabolism. We focus on phospholamban, sarcolipin and the calcium pump, and how they work together to trigger muscle relaxation. We take the following approaches. We are sequencing the phospholamban and sarcolipin genes in ~1000 University of Alberta heart failure patients. New disease-associated mutations that we identify will be studied using biochemical and structural biology methods. The goal is to develop a detailed molecular understanding of how mutations lead to heart disease. If we can fully understand these details, we may be able to better diagnose and treat patients presenting with heart disease.