Role of NLRP3 Inflammasomes in Hepatic Ischemia-reperfusion Injury

• Inoue Yoshiyuki

  Division of Inflammation Research Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan

• Sadatomo Ai

  Division of Inflammation Research Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan

• Takahashi Masafumi

  Division of Inflammation Research Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan

抄録

Increasing evidence indicates that inflammation plays an important role in the pathogenesis of hepatic ischemia-reperfusion (I/R) injury. However, it is still unclear how I/R stimuli induce inflammatory responses in the liver. NLRP3 is an intracellular pattern recognition receptor and a component of NLRP3 inflammasomes that can induce caspase-1 activation, and regulate the processing of a potent inflammatory cytokine, interleukin-1β (IL-1β). Several investigations have recently suggested that inflammatory responses are mediated through NLRP3 inflammasomes in hepatic I/R injury. On the other hand, we recently found that NLRP3 regulates neutrophil functions and contributes to hepatic I/R injury independently of inflammasomes. This review summarizes the basic information on NLRP3 inflammasomes and discusses inflammasome-dependent/independent roles of NLRP3 in the pathophysiology of hepatic I/R injury.

収録刊行物

• Inflammation and Regeneration

  Inflammation and Regeneration 35 (2), 061-068, 2015

  一般社団法人 日本炎症・再生医学会

キーワード

• cytokines
• inflammation
• liver
• leukocytes

詳細情報

• CRID: 1390282680234908672
• NII論文ID: 130005063949
• DOI: 10.2492/inflammregen.35.061
• ISSN: 18808190
• ISSN: 18809693
• Web Site: https://search.jamas.or.jp/link/ui/2016090838
• 本文言語コード: ja
• データソース種別:
  • JaLC
  • Crossref
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可