PMID- 36897552
OWN - NLM
STAT- MEDLINE
DCOM- 20230518
LR  - 20230518
IS  - 1573-2576 (Electronic)
IS  - 0360-3997 (Linking)
VI  - 46
IP  - 3
DP  - 2023 Jun
TI  - Therapeutic Potential of Targeting the NLRP3 Inflammasome in Rheumatoid 
      Arthritis.
PG  - 835-852
LID - 10.1007/s10753-023-01795-5 [doi]
AB  - NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is a 
      cytoplasmic multiprotein complex composed of the innate immune receptor protein 
      NLRP3, the adapter protein apoptosis-associate speck-like protein containing a 
      caspase recruitment domain (ASC), and the inflammatory protease cysteine-1. 
      Pathogen-associated molecular patterns (PAMPs) or other endogenous 
      danger-associated molecular patterns (DAMPs) activate the NLRP3 inflammasome. As 
      part of the innate immune response, activated NLRP3 promotes GSDMD-dependent 
      pyroptosis, and IL-1beta and IL-18 are released during inflammation. Aberrantly 
      activated NLRP3 is deeply involved in various inflammatory diseases. Due to its 
      interaction with adaptive immunity. NLRP3 inflammation has increasingly received 
      attention in autoimmune diseases. Rheumatoid arthritis (RA) is a classic 
      autoimmune disease, which mainly causes bone and cartilage damage. Elevated 
      levels of NLRP3 can be detected in the synovium of RA patients. NLRP3 
      overactivation is strongly associated with RA activity. Mouse models of 
      spontaneous arthritis has shown that NLRP3/IL-1beta axis is implicated in 
      periarticular inflammation in RA. In this review, we describe the current 
      understanding of NLRP3 activation in RA pathogenesis and dissect its impact on 
      innate and adaptive immunity. We also discuss the potential application of 
      specific inhibitors of NLRP3 to provide new therapeutic strategies for treating 
      RA.
CI  - (c) 2023. The Author(s), under exclusive licence to Springer Science+Business 
      Media, LLC, part of Springer Nature.
FAU - Gao, Jie
AU  - Gao J
AD  - Department of Rheumatology and Immunology, Division of Life Sciences and 
      Medicine, The First Affiliated Hospital of USTC, University of Science and 
      Technology of China, Hefei, 230001, People's Republic of China.
FAU - Zhang, Hongliang
AU  - Zhang H
AD  - Department of Rheumatology and Immunology, Division of Life Sciences and 
      Medicine, The First Affiliated Hospital of USTC, University of Science and 
      Technology of China, Hefei, 230001, People's Republic of China.
AD  - College of Medicine and Health, Lishui University, Liandu District, No. 1 Xueyuan 
      Road, Lishui, 323000, China.
FAU - Yang, Yanyan
AU  - Yang Y
AD  - Department of Rheumatology and Immunology, Division of Life Sciences and 
      Medicine, The First Affiliated Hospital of USTC, University of Science and 
      Technology of China, Hefei, 230001, People's Republic of China.
FAU - Tao, Jinhui
AU  - Tao J
AD  - Department of Rheumatology and Immunology, Division of Life Sciences and 
      Medicine, The First Affiliated Hospital of USTC, University of Science and 
      Technology of China, Hefei, 230001, People's Republic of China. 
      taojinhui@ustc.edu.cn.
LA  - eng
GR  - 81771774/National Natural Science Foundation of China/
GR  - 1708085MH191/the Natural Science Foundation of Anhui Province/
GR  - 201904a07020103/the Anhui Key Research and Development Foundation/
PT  - Journal Article
PT  - Review
DEP - 20230310
PL  - United States
TA  - Inflammation
JT  - Inflammation
JID - 7600105
RN  - 0 (Inflammasomes)
RN  - 0 (NLR Family, Pyrin Domain-Containing 3 Protein)
RN  - EC 3.4.22.36 (Caspase 1)
RN  - 0 (Nlrp3 protein, mouse)
SB  - IM
MH  - Animals
MH  - Mice
MH  - Inflammasomes/metabolism
MH  - NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
MH  - *Arthritis, Rheumatoid/drug therapy
MH  - *Autoimmune Diseases
MH  - Inflammation/drug therapy
MH  - Caspase 1
OTO - NOTNLM
OT  - IL-1beta
OT  - NLRP3
OT  - inflammasome
OT  - rheumatoid arthritis
EDAT- 2023/03/11 06:00
MHDA- 2023/05/18 06:42
CRDT- 2023/03/10 11:24
PHST- 2022/11/30 00:00 [received]
PHST- 2023/02/20 00:00 [accepted]
PHST- 2023/01/10 00:00 [revised]
PHST- 2023/05/18 06:42 [medline]
PHST- 2023/03/11 06:00 [pubmed]
PHST- 2023/03/10 11:24 [entrez]
AID - 10.1007/s10753-023-01795-5 [pii]
AID - 10.1007/s10753-023-01795-5 [doi]
PST - ppublish
SO  - Inflammation. 2023 Jun;46(3):835-852. doi: 10.1007/s10753-023-01795-5. Epub 2023 
      Mar 10.