Intracellular Signaling in Ischemia/Reperfusion Injury (IRI): From Mechanistic Insights to Therapeutic Options
- *Corresponding Author:
- Jakob Troppmair
Department of Visceral
Transplant and Thoracic Surgery
Innsbruck Medical University (IMU)
Innrain 66, 6020 Innsbruck, Austria
Tel: 0043 512 504 – 27819
E-mail: [email protected]
Received Date: November 15, 2011; Accepted Date: February 02, 2012; Published Date: February 07, 2012
Citation: Ashraf MI, Enthammer M, Haller M, Koziel K, Hermann M, et al. (2012) Intracellular Signaling in Ischemia/Reperfusion Injury (IRI): From Mechanistic Insights to Therapeutic Options. J Transplant Technol Res S3: 002. doi: 10.4172/2161-0991.S3-002
Copyright: © 2012 Ashraf MI, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Transplantation of solid organs is invariably linked to a disruption of oxygen and nutrient supply. Damage initiated in the ischemic period is greatly enhanced during reperfusion. In particular the excessive production of reactive oxygen species (ROS) plays a key role in the development of ischemia/reperfusion injury (IRI), which in the clinical setting is difficult to control through the use of antioxidants. Ischemia/reperfusion (IR) is also marked by the activation of intracellular signaling pathways, which may have protective but also damaging effects. Modulating intracellular signaling thus may hold the promise to prevent or minimize IRI. Most intriguingly, some of these pathways have been shown recently to control mitochondrial events, including the production of ROS. Understanding this cytoplasmic/ mitochondrial crosstalk will be the basis for the development of novel approaches for the prevention of IRI.