Therapeutic strategies in inflammasome mediated diseases of the liver

Rafaz Hoque, Yoram Vodovotz, Wajahat Mehal*

*Corresponding author for this work

Research output: Contribution to journalComment/debate

30 Scopus citations

Abstract

Tissue stress and cell death result in inflammation even in the absence of pathogens. Such sterile inflammation is dependent on a cytosolic complex of proteins inside immune cells termed the inflammasome. This complex converts two groups of extracellular signals into an inflammatory response via activation of caspase-1 and secretion of IL-1β and IL-18. Group 1 signals are typically TOLL like receptor agonists and result in transcriptional upregulation of inflammasome components and pro-cytokines. Group 2 signals are diverse, ranging from uric acid to ATP, and lead to assembly and activation of the inflammasome complex. Inflammasome components are required for a wide range of acute and chronic pathologies, including experimental alcoholic and non-alcoholic steatohepatitis, and drug-induced liver injury. Collectively, group 1 and 2 signals, inflammasome components, and cytokine receptors provide a rich source of therapeutic targets. Many of the advances in the field have come from standard reductionist experiments. Progress in the understanding of complex human systems will, however, be dependent on novel strategies such as systems analysis, which analyze large data sets to provide new insights.

Original languageEnglish
Pages (from-to)1047-1052
Number of pages6
JournalJournal of Hepatology
Volume58
Issue number5
DOIs
StatePublished - May 2013
Externally publishedYes

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