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.
Highlights
Osteoarthritis (OA), as an age-related degenerative joint disease, presents with physical pain and disability in patients
We focus on chondrocyte inflammation, apoptosis, pyroptosis, and autophagy, and analyze the correlation between these phenotypes and cartilage degradation in OA
From the perspective of apoptosis, pyroptosis, and autophagy, we discuss the possible association between P2X7 receptor (P2X7R), cartilage degradation, and inflammatory factor release in OA
Summary
Osteoarthritis (OA), as an age-related degenerative joint disease, presents with physical pain and disability in patients. From the perspective of apoptosis, pyroptosis, and autophagy, we discuss the possible association between P2X7R, cartilage degradation, and inflammatory factor release in OA. Exercise reduced the expression levels of P2X7R, NLRP3, caspase-1, and IL-1β in plasma caused by a high-fat diet in Sprague Dawley rats, inhibiting inflammation and apoptosis, enhancing autophagy, and reducing myocardial damage (Chen et al, 2019).
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