Hepatic I/R (ischaemia/reperfusion) injury occurs in a variety of clinical settings including transplantation, elective liver resections and trauma. One of the challenges in studying the pathophysiology of I/R injury is the fact that the liver plays a central role in a variety of metabolic pathways in addition to governing aspects of immune surveillance and tolerance. The pathways activated in response to insults as varied as toxins, microbial and endogenous ligands and I/R may share common elements. The multiple intracellular signalling cascades involved in this process and the initiating events are still under investigation. Recent work on the role of TLRs (Toll-like receptors) in I/R injury has elucidated some of the more proximal signalling events in the pathway. In addition to the well-established role of signalling molecules such as NO (nitric oxide) in mediating damage or protection following hepatic I/R, more recent studies have focused on the participation of endogenous danger signals or DAMPs (damage-associated molecular patterns) such as HMGB1 (high-mobility group box 1). The complex interplay between HMGB1, TLRs and the many intracellular signalling molecules and pathways is illustrative of how our understanding of hepatic I/R injury is continually evolving.
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Conference Article| October 25 2006
Linking proximal and downstream signalling events in hepatic ischaemia/reperfusion injury
T.R. Billiar 1
1Department of Surgery, University of Pittsburgh, School of Medicine, 200 Lothrop Street, Presbyterian Hospital F1200, Pittsburgh, PA 15213, U.S.A.
1To whom correspondence should be addressed (email firstname.lastname@example.org).
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Publisher: Portland Press Ltd
Received: August 10 2006
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2006 The Biochemical Society
G. Jeyabalan, A. Tsung, T.R. Billiar; Linking proximal and downstream signalling events in hepatic ischaemia/reperfusion injury. Biochem Soc Trans 1 October 2006; 34 (5): 957–959. doi: https://doi.org/10.1042/BST0340957
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