Published online Jun 28, 2019. doi: 10.3748/wjg.v25.i24.3044
Peer-review started: March 20, 2019
First decision: April 4, 2019
Revised: April 27, 2019
Accepted: June 1, 2019
Article in press: June 1, 2019
Published online: June 28, 2019
Core tip: Liver fibrosis is a pathological tissue repair process characterized by excessive deposition of extracellular matrix in the liver, accompanied by inflammation, and eventually progresses to cirrhosis. Several recent reports have shown that effective treatment can reverse liver fibrosis, which is associated with inactivation of hepatic stellate cells (HSCs) and multiple signaling pathways. NOD-like receptor (NLR) family, caspase activation and recruitment domain (CARD) domain containing 5/NOD27/CLR16.1 (NLRC5) is the largest member of the NLR family and is highly expressed in immune tissues or organs such as the spleen, lung, thymus, and liver, mediating inflammation inhibition and antiviral response. This study aimed to investigate the role of NLRC5 in activating and devitalization of HSCs and its mechanism. The results demonstrate that NLRC5 may be involved in the development and reversal of liver fibrosis by negative regulation of nuclear factor-κB.