Dr. Stephen Archer

Stephen Archer

613.533.6327 x.36327
  • Clinician Scientist, KGHRI
  • Head, Department of Medicine, Queen’s University
  • Tier 1 Canada Research Chair in Mitochondrial Dynamics and Translational Medicine

Pulmonary hypertension, cancer, mitochondrial dynamics, mitochondrial metabolism, oxygen-sensing, aortic diseases and valvular heart diseases. 


Dr. Archer spent 12 years as a Chief of Cardiology at the University of Alberta and then at the University of Chicago before returning to his medical school roots in 2012 to Queen’s University. He now serves as the Head of Medicine at Queen’s University, Hotel Dieu Hospital, Kingston General Hospital, and Providence Care.  Dr. Archer has published over 220 peer-reviewed articles in leading journals and has given ~300 invited lectures including plenary session lectures at the American Heart Association Meeting and numerous named lectureships.  He is also been an author of several key guideline documents, including the AHA 2009 guidelines on pulmonary hypertension and the 2010 guidelines on management of submassive venothromboembolism.


Education and Honours
  • Distinguished Scientist Award, American Heart Association (2016)
  • Chicago American Heart Association Coeur d’Or recipient (2013)

O2-sensing: Hypoxic pulmonary vasoconstriction (HPV) matches perfusion to ventilation. We study the “RedoxTheory” of HPV. The identity and function of a mitochondrial O2-sensor in smooth muscle cell and its effects on ion channels and rho kinase is assessed.

Pulmonary arterial hypertension (PAH): PAH is an obliterative pulmonary vasculopathy resulting in death from right ventricular (RV) failure. The cancer-like proliferation/apoptosis imbalance in the vasculature and RV is studied, focusing on: 1) HIF-1a and pyruvate dehydrogenase kinase (PDK) activation 2) epigenetic silencing of SOD2 3) disordered mitochondrial fusion and fission 4) RV microvascular rarefaction and cancer-like metabolism.

Metabolism, fusion and fission in cancer: The lab investigates mitochondrial and metabolic therapies for cancer, including the role of DRP-1-mediated fission and mitofusin-2-mediated fusion.

Ductus arteriosus (DA): O2-induced constriction of human DA results from PO2-dependent inhibition of O2-sensitive, Kv channels in myocytes. The role of mitochondrial fission in redox-based O2-sensing and implications for DA constriction/closure are studied.