Linking proximal and downstream signalling events in hepatic ischaemia/reperfusion injury

G. Jeyabalan, A. Tsung, T. R. Billiar*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


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.

Original languageEnglish
Pages (from-to)957-959
Number of pages3
JournalBiochemical Society Transactions
Issue number5
StatePublished - Nov 2006
Externally publishedYes


  • Damage-associated molecular pattern (DAMP)
  • Dendritic cell
  • Ischaemia/reperfusion injury
  • Nitric oxide synthase
  • Toll-like receptor (TLR)
  • high-mobility group box 1 (HMGB1)


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