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Abundant evidence indicted that P2X7 receptor show a essential role in human health and some human diseases including hypertension, atherosclerosis, pulmonary inflammation, tuberculosis infection, psychiatric disorders, and cancer. P2X7 receptor also has an important role in some central nervous system diseases such as neurodegenerative disorders. Recently, more research suggested that P2X7 receptor also plays a crucial role in bone and joint diseases. But the effect of P2X7 receptor on skeletal and joint diseases has not been systematically reviewed. In this article, the role of P2X7 receptor in skeletal and joint diseases is elaborated. The activation of P2X7 receptor can ameliorate osteoporosis by inducing a fine balance between osteoclastic resorption and osteoblastic bone formation. The activation of P2X7 receptor can relieve the stress fracture injury by increasing the response to mechanical loading and inducing osteogenesis. But the activation of P2X7 receptor mediates the cell growth and cell proliferation in bone cancer. In addition, the activation of P2X7 receptor can aggravate the process of some joint diseases such as osteoarthritis, rheumatoid arthritis, and acute gouty arthritis. The inhibition of P2X7 receptor can alleviate the pathological process of joint disease to some extent. In conclusion, P2X7 receptor may be a critical regulator and therapeutic target for bone and joint diseases.

Laminar shear stress is considered to improve endothelial cell (EC) function. However, the underlying mechanism is unclear. Autophagy has been found to protect cell survival under stress. In this study, the effect of laminar shear stress on EC autophagy and its potential mechanism were explored. The autophagic markers, Beclin 1 and LC3 II, in human umbilical vascular endothelial cells increased after laminar shear stress treatment. Meanwhile, the autophagic substrate, p62, decreased. The protein level of Rab4 increased under laminar shear stress. When pretreated with Rab4 siRNA, the increased levels of Beclin 1 and LC3 II were attenuated and p62 levels significantly increased. In addition, the MCP level and the adhesion of monocytes were also obviously increased by Rab4 siRNA. Laminar shear stress upregulated Rab4 expression, which contributed to improved EC autophagy and function.

The expression of PAR-1 is regulated by thrombin that induces the expression of TGF-β1 to promote airway remodeling via PAR-1 in OVA-allergic rats.