Figure 1

The control of caspase-1 activation by [K⁺] levels. The cell gauges danger by monitoring its intracellular potassium levels. At normal [K⁺], caspase-1 activation is inhibited, unless IPAF is engaged. In response to inflammatory triggers and infections, potassium channels on the plasma membrane open resulting in potassium efflux, an alarm signal that induces the formation of caspase-1 activation platforms. At intermediate [K⁺] concentrations, Nalps bind ASC and caspase-1 to form the inflammasome, in which caspase-1 is activated transiently, leading to controlled inflammation. At sufficiently low [K⁺] levels, ASC binds caspase-1 directly and forms the pyroptosome, in which caspase-1 is fully activated leading to pyroptosis and a burst of cytokine release