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. Author manuscript; available in PMC: 2021 Apr 1.
Published in final edited form as: FASEB J. 2020 Feb 21;34(4):5465–5482. doi: 10.1096/fj.201903287R

Figure 10. A proposed mechanism of P2X4 receptor-mediated exacerbation of ischemic AKI.

Figure 10.

Our data show that P2X4 activation in renal proximal tubules induce NLRP3 inflammasome synthesis. Dying or necrotic renal cells release ATP to extracellular space. Opening of the P2X4 channels in response to extracellular ATP leads to K+ efflux and Ca++ influx potentially driving reactive oxygen species and NLRP3 inflammasome assembly. Subsequent caspase 1 activation, cleavage, and release of active IL-1β can induce additional renal tubular apoptosis and inflammation as well as systemic inflammatory response.