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. 2022 Mar 11;27(6):1838. doi: 10.3390/molecules27061838

Figure 1.

Figure 1

P2X7R modulation of β-cell pro-inflammatory functions. Hyperglycemia promotes eATP release and P2X7R-dependent K+ efflux and Ca2+ influx into the β-cells. Ca2+ overload promotes mitochondrial dysfunction, reactive oxygen species (ROS) generation, inhibition of ATP synthesis, and eventually triggers apoptosis. Moreover, intracellular K+ decrease induces the assembly of the NLRP3 inflammasome, promotes IL-1β release and further accelerates β-cell apoptosis.