Pyroptosis in Periprosthetic Osteolysis

被引:10
|
作者
Yin, Jian [1 ,2 ]
Yin, Zhaoyang [3 ]
Lai, Peng [4 ]
Liu, Xinhui [2 ]
Ma, Jinzhong [1 ,2 ,4 ]
机构
[1] Nanjing Med Univ, Shanghai Gen Hosp, Dept Orthoped, Shanghai 201600, Peoples R China
[2] Nanjing Med Univ, Affiliated Jiangning Hosp, Dept Orthoped, Nanjing 211100, Peoples R China
[3] Xuzhou Med Univ, Affiliated Lianyungang Hosp, The Peoples Hosp Lianyungang 1, Dept Orthoped, Lianyungang 222000, Peoples R China
[4] Shanghai Jiao Tong Univ, Shanghai Gen Hosp, Sch Med, Dept Orthoped, Shanghai 201600, Peoples R China
基金
中国国家自然科学基金;
关键词
periprosthetic osteolysis; aseptic loosening; NLRP3; pyroptosis; inflammation; PARTICLE-INDUCED OSTEOLYSIS; NLRP3; INFLAMMASOME; OSTEOCLAST DIFFERENTIATION; CATHEPSIN-B; OSTEOGENIC ACTIVITY; KNEE ARTHROPLASTY; KETOGENIC DIET; REVISION HIP; CELL-DEATH; EXPRESSION;
D O I
10.3390/biom12121733
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Periprosthetic osteolysis (PPO) along with aseptic loosening (AL) caused by wear particles after artificial joint replacement is the key factor in surgical failure and subsequent revision surgery, however, the precise molecular mechanism underlying PPO remains unclear. Aseptic inflammation triggered by metal particles, resulting in the imbalance between bone formation by osteoblasts and bone resorption by osteoclasts may be the decisive factor. Pyroptosis is a new pro-inflammatory pattern of regulated cell death (RCD), mainly mediated by gasdermins (GSDMs) family, among which GSDMD is the best characterized. Recent evidence indicates that activation of NLRP3 inflammasomes and pyroptosis play a pivotal role in the pathological process of PPO. Here, we review the pathological process of PPO, the molecular mechanism of pyroptosis and the interventions to inhibit the inflammation and pyroptosis of different cells during the PPO. Conclusively, this review provides theoretical support for the search for new strategies and new targets for the treatment of PPO by inhibiting pyroptosis and inflammation.
引用
收藏
页数:16
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