Literature DB >> 33644066

The P2X7 Receptor in Osteoarthritis.

Zihao Li1, Ziyu Huang2, Lunhao Bai1.   

Abstract

Osteoarthritis (OA) is the most common joint disease. With the increasing aging population, the associated socio-economic costs are also increasing. Analgesia and surgery are the primary treatment options in late-stage OA, with drug treatment only possible in early prevention to improve patients' quality of life. The most important structural component of the joint is cartilage, consisting solely of chondrocytes. Instability in chondrocyte balance results in phenotypic changes and cell death. Therefore, cartilage degradation is a direct consequence of chondrocyte imbalance, resulting in the degradation of the extracellular matrix and the release of pro-inflammatory factors. These factors affect the occurrence and development of OA. The P2X7 receptor (P2X7R) belongs to the purinergic receptor family and is a non-selective cation channel gated by adenosine triphosphate. It mediates Na+, Ca2+ influx, and K+ efflux, participates in several inflammatory reactions, and plays an important role in the different mechanisms of cell death. However, the relationship between P2X7R-mediated cell death and the progression of OA requires investigation. In this review, we correlate potential links between P2X7R, cartilage degradation, and inflammatory factor release in OA. We specifically focus on inflammation, apoptosis, pyroptosis, and autophagy. Lastly, we discuss the therapeutic potential of P2X7R as a potential drug target for OA.
Copyright © 2021 Li, Huang and Bai.

Entities:  

Keywords:  P2X7 receptor; apoptosis; autophagy; inflammation; osteoarthritis; pyroptosis

Year:  2021        PMID: 33644066      PMCID: PMC7905059          DOI: 10.3389/fcell.2021.628330

Source DB:  PubMed          Journal:  Front Cell Dev Biol        ISSN: 2296-634X


  246 in total

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8.  NF-κB Restricts Inflammasome Activation via Elimination of Damaged Mitochondria.

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Journal:  Cell Death Dis       Date:  2019-11-25       Impact factor: 8.469

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1.  Metformin alleviates osteoarthritis in mice by inhibiting chondrocyte ferroptosis and improving subchondral osteosclerosis and angiogenesis.

Authors:  Jiangbo Yan; Gangning Feng; Long Ma; Zhirong Chen; Qunhua Jin
Journal:  J Orthop Surg Res       Date:  2022-06-28       Impact factor: 2.677

2.  The P2X7 purinergic receptor in intervertebral disc degeneration.

Authors:  Letizia Penolazzi; Leticia S Bergamin; Elisabetta Lambertini; Valentina V Poma; Alba C Sarti; Pasquale De Bonis; Francesco Di Virgilio; Roberta Piva
Journal:  J Cell Physiol       Date:  2021-10-19       Impact factor: 6.513

3.  Moderate-intensity exercise alleviates pyroptosis by promoting autophagy in osteoarthritis via the P2X7/AMPK/mTOR axis.

Authors:  Zihao Li; Ziyu Huang; He Zhang; Jinghan Lu; Yicheng Tian; Shang Piao; Zhiming Lin; Lunhao Bai
Journal:  Cell Death Discov       Date:  2021-11-10

4.  Metformin reduces chondrocyte pyroptosis in an osteoarthritis mouse model by inhibiting NLRP3 inflammasome activation.

Authors:  Jiangbo Yan; Dong Ding; Gangning Feng; Yong Yang; Yong Zhou; Long Ma; Haohui Guo; Zhidong Lu; Qunhua Jin
Journal:  Exp Ther Med       Date:  2022-01-17       Impact factor: 2.447

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Authors:  Yonggang Ma; Ran Di; Hongyan Zhao; Ruilong Song; Hui Zou; Zongping Liu
Journal:  Mol Med Rep       Date:  2022-03-10       Impact factor: 2.952

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Authors:  Rigbat Rozi; Yubo Zhou; Kai Rong; Pingbo Chen
Journal:  J Orthop Surg Res       Date:  2022-10-15       Impact factor: 2.677

7.  IRE1-mTOR-PERK Axis Coordinates Autophagy and ER Stress-Apoptosis Induced by P2X7-Mediated Ca2+ Influx in Osteoarthritis.

Authors:  Zihao Li; Ziyu Huang; He Zhang; Jinghan Lu; Yingliang Wei; Yue Yang; Lunhao Bai
Journal:  Front Cell Dev Biol       Date:  2021-06-17

Review 8.  Targeting Cell Death: Pyroptosis, Ferroptosis, Apoptosis and Necroptosis in Osteoarthritis.

Authors:  Jian Yang; Shasha Hu; Yangyang Bian; Jiangling Yao; Dong Wang; Xiaoqian Liu; Zhengdong Guo; Siyuan Zhang; Lei Peng
Journal:  Front Cell Dev Biol       Date:  2022-01-18
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