Medical College of Wisconsin
Medical College of Wisconsin Medical College of Wisconsin
Staff Collaborate Conference Room
David F. Stowe, MD, PhD
David Stowe, MD, PhD

David Stowe, MD, PhD

Professor

Contact Information

Education

Diploma, Zoology, Free University of Berlin - Berlin, Germany, 1966
BA, Zoology, Indiana University - Bloomington, IN, 1968
MA, Cell Biology, Indiana University - Bloomington, IN, 1970
PhD, Physiology, Michigan State University - East Lansing, MI, 1974
Postdoc, Cardiac Physiology, University of California - San Francisco, CA, 1974–1976
MD, Medical College of Wisconsin - Milwaukee, WI, 1979-1983
Residency, Anesthesiology, Medical College of Wisconsin - Milwaukee, WI, 1983–1987
Visit the Stowe Lab webpage

Research Interests

  1. Mechanisms for and protection against cardiac ischemia-reperfusion injury
  2. Identification and function of mitochondrial ion channels and ion exchangers
  3. Assessment of mitochondrial transmembrane calcium fluxes and sequestration
  4. Mitochondrial protection against subacute liver ischemia and traumatic brain injury

Publications

Publications of David F. Stowe MD, PhD from the Faculty Collaboration Database

The Stowe laboratory is currently active in several areas:

  • Mechanism and timing of activation of cardiac mitochondrial small and large K+-sensitive Ca2+ (SKCa and BKCa) channels; their protective role against acute cardiac injury; identification of specific mitochondrial SKCa splice variants in several species, including human; and the molecular and biophysical mechanisms underlying protection by opening of these mitochondrial channels.
  • Mitigation of Ca2+ dysregulation and excess reactive oxygen species emission in acute cardiac injury.
  • Regulation of mitochondrial Ca2+ flux through Ca2+ channels and Ca2+ exchangers with H+, K+ and Na+; and exploration of dynamic mitochondrial Ca2+ buffering mechanisms.
  • Ischemia-induced nitration of nucleotide transporters VDAC and ANT on promoting mitochondrial and cell damage with identification of specific residues that are causative in impeding nucleotide transport and mitochondrial dysfunction.
  • Mitochondrial function in liver cells during the perioperative transplant period.
  • Mitochondrial function in glial and neurons after subacute tramatic brain injury.

Collaborators include: AKS Camara, WM Kwok, C Pawela, A Geurts, J Hong, MY Yang, J Mishra, Q Cheng, L Keguo, JS Heisner, D Schwabe, and pre- and post doctoral students.