Paul T. Schumacker, PhD, MEng, ATSF, FERS

Basic and Preclinical Science
Injury, Repair, and Regeneration
Schumacker Laboratory
Pronouns: He, Him, His

“If you need to do something new, talk to people who already know how to do it.”

Research Interests

  • Hypoxia
  • Cancer
  • Metabolism
  • Mitochondria
  • Cell Signaling

Biography

  • Patrick M. Magoon Distinguished Professor in Neonatal Research, Ann & Robert H. Lurie Children’s Hospital of Chicago
  • Professor of Pediatrics, Cell and Molecular Biology, and Medicine, Northwestern University Feinberg School of Medicine

Education and Background

  • Fellowship, Section of Respiratory Physiology, University of California San Diego 1978-1983
  • PhD, Physiology, Albany Medical College 1980
  • MEng, Biomedical Engineering, Rensselaer Polytechnic Institute 1976
  • BS, Biomedical Engineering, Rensselaer Polytechnic Institute 1974

Research Highlights

MITOCHONDRIAL FUNCTIONS REGULATE CARDIOMYOCYTE PROLIFERATION

This project examines the role of mitochondria in regulating cell proliferation in the heart. Newborn heart cells are capable of undergoing cell division, which can repair heart damage with new muscle cells during the perinatal period. However, soon after birth, these cells transition from fetal myocytes into adult heart cells that have lost the ability to divide. After this transition has occurred, damaged hearts are repaired with scar tissue, which interferes with normal contraction and can contribute to heart failure. We have discovered that mitochondria regulate the heart cell's transition from mitosis-competent into a post-mitotic state. During that transition, the heart cells switch from a fetal reliance on glycolysis to the adult reliance on oxidative phosphorylation. Forcing the adult heart cells to return to a reliance on glycolysis causes a re-awakening of their ability to undergo cell division, and the hearts grow in size by turning on gene pathways associated with cardiac development. This response, when activated concurrently with the induction of ischemic injury, results in the migration of new heart cells into the region of cell damage, opening the possibility that this response could be used to repair under-developed left hearts in newborns, or to repair ischemic damage in adult hearts.

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