Research Group

  • Prof. Victor Laubach, Principal Investigator
  • Dr Zequan Yang, Research Associate
  • Dr Sheila Hammond, Laboratory Technician
  • Dr Tony Herring, Laboratory Technician
  • Prof. Irving Kron, Collaborator
  • Prof Joel Linden, Collaborator
  • Prof. Mark Stoler, Collaborator
  • Prof. Katya Ravid, Collaborator
  • Prof. Jurgen Schnermann, Collaborator


  • University of Virginia, Charlottesville, USA


  • Prevention of Lung Transplant Injury by Adenosine Receptor Activation

For many forms of end-stage lung disease, the only treatment is lung transplantation. Unfortunately, reperfusion injury, which occurs rapidly after transplant, affects up to 40% of lung transplant patients, resulting in significant morbidity and mortality. Our goal is to study mechanisms of lung reperfusion injury to develop novel preventative therapies. In post-transplant reperfusion injury, adenosine production is known to be a protective agent due to its anti-inflammatory effects. Adenosine can exert its effects by activating any of four different targets (receptors) in the lung. Our laboratory has shown that specific activation of the adenosine 2A receptor significantly reduces reperfusion injury.However, we know very little about the role of the other three receptors (A1, A2B, and A3) in reperfusion injury. This project will determine the role of each adenosine receptor in lung reperfusion injury using both mouse and pig models. We will test if the adenosine 2A receptor is the primary receptor which provides the protective effects of adenosine during reperfusion injury. Using the clinically relevant pig lung transplant model, we will also test if pharmacologic activation of the adenosine 2A receptor in the donor lung will confer optimal protection from reperfusion injury. This project has strong implications for the advancement of therapeutic drugs that directly target and activate adenosine 2A receptors for the prevention of post-transplant reperfusion injury.