Ischemic preconditioning modulates ROS to confer protection in liver ischemia and reperfusion

Authors

  • Phillip Bystrom Western Michigan University, Homer Stryker M.D. School of Medicine Department of Biomedical Sciences
  • Nicole Foley Western Michigan University, Homer Stryker M.D. School of Medicine Department of Biomedical Sciences
  • Luis Toledo-Pereyra Western Michigan University, Homer Stryker M.D. School of Medicine Department of Surgery
  • Kelly Quesnelle Western Michigan University, Homer Stryker M.D. School of Medicine Department of Biomedical Sciences

DOI:

https://doi.org/10.17179/excli2017-166

Keywords:

ischemia, reperfusion injury, liver, preconditioning, reactive oxygen species, oxidative stress

Abstract

Ischemia reperfusion (IR) injury is a significant cause of morbidity and mortality in liver transplantation. When oxygen is reintroduced to the liver graft it initiates a cascade of molecular reactions leading to the release of reactive oxygen species (ROS) and pro-inflammatory cytokines. These soluble mediators propagate a sterile immune response to cause significant tissue damage. Ischemic preconditioning (IPC) is one method that reduces hepatocellular injury by altering the immune response and inhibiting the production of ROS. Studies quantifying the effects of IPC in humans have demonstrated an improved liver enzyme panel in patients receiving grafts pretreated with IPC as compared to patients receiving the standard of care. In our review, we explore current literature in the field in order to describe the mechanism through which IPC regulates the production of ROS and improves IR injury.

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Published

2017-04-07

How to Cite

Bystrom, P., Foley, N., Toledo-Pereyra, L., & Quesnelle, K. (2017). Ischemic preconditioning modulates ROS to confer protection in liver ischemia and reperfusion. EXCLI Journal, 16, 483–496. https://doi.org/10.17179/excli2017-166

Issue

Vol. 16 (2017)

Section

Review articles

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