TY - JOUR
T1 - Relevance of the NLRP3 inflammasome in the pathogenesis of chronic liver disease
AU - Wu, Xiaoqin
AU - Dong, Lei
AU - Lin, Xianhe
AU - Li, Jun
N1 - Publisher Copyright:
© 2017 Wu, Dong, Lin and Li.
PY - 2017/12/12
Y1 - 2017/12/12
N2 - Inflammation is a common characteristic of chronic liver disease (CLD). Inflammasomes are multiprotein complexes that can sense and recognize various exogenous and endogenous danger signals, eventually activating interleukin (IL)-1β and IL-18. The sensor component of the inflammasome system is a nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs). The NLRs family pyrin domain containing 3 (NLRP3) inflammasome has been involved in the initiation and progression of CLD. However, the molecular mechanisms by which it triggers liver inflammation and damage remain unclear. Here, we focus on recent advances on the potential role of NLRP3 inflammasome activation in the progression of CLD, including viral hepatitis, non-alcoholic steatohepatitis and alcoholic liver disease, and in particular, its ability to alleviate liver inflammation in animal models. Additionally, we also discuss various pharmacological inhibitors identifying the NLRP3 inflammasome signaling cascade as novel therapeutic targets in the treatment of CLD. In summary, this review summarizes the relevance of the NLRP3 inflammasome in the initiation and progression of CLD, and provides critical targets to suppress the development of CLD in clinical management.
AB - Inflammation is a common characteristic of chronic liver disease (CLD). Inflammasomes are multiprotein complexes that can sense and recognize various exogenous and endogenous danger signals, eventually activating interleukin (IL)-1β and IL-18. The sensor component of the inflammasome system is a nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs). The NLRs family pyrin domain containing 3 (NLRP3) inflammasome has been involved in the initiation and progression of CLD. However, the molecular mechanisms by which it triggers liver inflammation and damage remain unclear. Here, we focus on recent advances on the potential role of NLRP3 inflammasome activation in the progression of CLD, including viral hepatitis, non-alcoholic steatohepatitis and alcoholic liver disease, and in particular, its ability to alleviate liver inflammation in animal models. Additionally, we also discuss various pharmacological inhibitors identifying the NLRP3 inflammasome signaling cascade as novel therapeutic targets in the treatment of CLD. In summary, this review summarizes the relevance of the NLRP3 inflammasome in the initiation and progression of CLD, and provides critical targets to suppress the development of CLD in clinical management.
KW - Alcoholic liver disease
KW - Inflammasome
KW - Inflammation
KW - Non-alcoholic steatohepatitis
KW - Viral hepatitis
UR - http://www.scopus.com/inward/record.url?scp=85037985824&partnerID=8YFLogxK
U2 - 10.3389/fimmu.2017.01728
DO - 10.3389/fimmu.2017.01728
M3 - Review article
AN - SCOPUS:85037985824
SN - 1664-3224
VL - 8
JO - Frontiers in Immunology
JF - Frontiers in Immunology
IS - DEC
M1 - 1728
ER -