Dr. Julio Cesar Batista Ferreira

Dr. Ferreira received his PhD in Cardiovascular Physiology from the University of Sao Paulo. As a postdoctoral fellow at Stanford, he worked on protein-protein interactions that regulate mitochondrial dynamics. He firsst characterized the role of a calcium-sensitive PKC (PKCβII) in mitochondrial dynamics through mitofusin 1 and developed a selective peptide that blocks this interaction and improves heart failure outcome. Dr. Ferreira also helped to elucidate the role of mitochondrial dynamics in cardiac ischemia-reperfusion injury where excessive mitochondrial fission contributes to long-term cardiac dysfunction. At University of Sao Paulo since 2012, his lab set out to study the mitochondrial aldehyde dehydrogenase 2 and its association with human diseases. This enzyme plays a critical role in detoxifying aldehydes that accumulate through oxidative stress and to which we are exposed from the environment. They provided evidence that activating ALDH2, using a small compound discovered by Mochly-Rosen lab (Alda-1), is sufficient in protect against aldehyde-induced mitochondrial dysfunction and improve heart failure outcome. They also demonstrated that ALDH2 activator counteracts the deleterious effects of an ALDH2 inactivating mutation (termed ALDH2*2) during ischemia-reperfusion injury. More recently, Ferreira’s lab has been studying the impact of exercise on muscle fitness in health and disease. His lab has shown that exercise promotes a cardiac and skeletal muscle anti-remodeling effect followed by improved outcome in different physiological and pathological conditions. They provided evidence that the positive impact of exercise on cardiac muscle occurs thorough a better clearance of damaged and dysfunctional mitochondria; therefore recovering the synergy between cardiac mitochondrial quality control and bioenergetic efficiency in heart failure.