Stephen L. Archer, MD, FAHA, is the Tier 1 Canada Research Chair in Mitochondrial Dynamics and Translational Medicine, Professor and Head, Department of Medicine at Queen’s University in Kingston, Ontario, Canada
Dr. Archer is a Canadian and graduate of Queen’s University. After interning at the Royal Columbian Hospital, he completed his training in Medicine and Cardiology at the University of Minnesota. He worked at the Minneapolis Veterans Affairs Medical Center. Subsequently he was Chief of Cardiology at the University of Alberta and University of Chicago. He is currently Head of Medicine at Queen’s University. He holds a Tier 1 Canada Research Chair in Mitochondrial Dynamics and Translational Medicine, has more than 230 publications, and is particularly proud of his many successful trainees.
A longstanding AHA volunteer he has chaired many peer review committees and served as president of the Chicagoland AHA Board. His Discoveries include:
- Hypoxic pulmonary vasoconstriction and O2-induced ductus arteriosus constriction: With Weir and Thébaud established that O2-induced changes in mitochondrial function alter H2O2 production, which regulates ion channels and enzymes and thus vascular tone.
- cGMP-induced vasodilation: cGMP activates protein kinase G, which opens potassium channels, thereby hyperpolarizing membrane potential and causes vasodilatation.
- Sildenafil as Pulmonary Arterial Hypertension (PAH) therapy: With Michelakis showed the acute and chronic benefits of sildenafil in PAH.
- Epigenetics of PAH: Methylation of the superoxide dismutase (SOD2) gene decreases H2O2 production causing normoxic HIF-1? activation. The resulting glycolytic metabolism and mitochondrial fragmentation are amenable to therapy.
- Mitochondrial dynamics in human diseases: With Sharp and Rehman showed that nuclear and mitochondrial division are coordinated by cyclin B-CDK1, which triggers mitosis and activates dynamin-related protein 1. This promotes the proliferative, apoptosis-resistant phenotype of PAH and cancer and can be therapeutically targeted. Fission also mediates cardiac ischemia- reperfusion injury.
- Mitochondrial-metabolic abnormalities in PAH and cancer: With Michelakis showed that pyruvate dehydrogenase kinase (PDK)-mediated inhibition of pyruvate dehydrogenase promotes aerobic glycolysis, suppresses apoptosis and drives proliferation. PDK inhibitors regress cancer and PAH.