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Kostas Pantopoulos

Kostas Pantopoulos, PhD

Molecular & Regenerative Medicine

Anemias, Ferritin, Ferroportin, Hemochromatosis, Hepcidin, Iron metabolism, Iron regulatory proteins, Metabolic disorders, Transferrin receptor
  • Senior Investigator, Lady Davis Institute for Medical Research
  • Professor, Department of Medicine, McGill University

Contact details

(514) 340-8260 ext. 25293
kostas.pantopoulos@mcgill.ca

Snapshot

Iron homeostasis is critical for health and its disruption leads to disease. Thus, iron-deficiency is the most prevalent medical condition affecting one quarter of the world’s population, while iron overload is a hallmark of inherited disorders such as hereditary hemochromatosis or thalassemias. Deregulation of iron metabolism also occurs in common inflammatory, infectious, metabolic, cardiovascular and neurological diseases, as well as in cancer.

The long-term goals of our research program are to:

  • Study mechanisms of cellular and systemic iron homeostasis.
  • Understand how iron homeostasis is disrupted under pathological conditions.
  • Develop new therapies for the treatment of iron-related disorders.

Important Links :

See Kostas Pantopoulos' publications on PubMed

Major Research Activities

Kostas Pantopoulos’ ongoing projects in the laboratory focus on the following specific areas:

  • Study mechanisms for iron sensing and iron traffic in the liver, which result in activation of the iron hormone hepcidin, and understand pathophysiological implications of hepcidin deregulation. To this end, we are utilizing mice with tissue-specific disruption of transferrin receptor 1 (Tfr1), the cellular iron gate, and Hjv-/- mice with disruption of hemojuvelin (Hjv), an upstream regulator of hepcidin.
  • Explore regulatory connections between iron and intermediary metabolism. We are utilizing mouse models with defective iron homeostasis, such as Irp1-/- or hepatocyte-specific Tfr1-/- mice, and we are analyzing their responses to metabolic challenges.
  • Investigate iron metabolism in cancer. We are utilizing mouse models with tissue-specific or global disruption of iron metabolism proteins (Tfr1, Hjv, IRP1 or IRP2) to study implications in carcinogenesis and tumor growth.

Recent Publications and References