In this issue of Blood, Dinarvand and colleagues identify polyphosphate (polyP) as a potent mediator of proinflammatory effects induced by nuclear proteins such as histone H4 and high mobility group box 1 (HMGB1). Coagulation, platelet activation, and inflammation are intricately linked and regulatory mechanisms ensure a balanced response to infection and inflammation. Not only do these observations promote polyP to the ranks of an all-round proinflammatory and procoagulant agent, but also protection by activated protein C (APC) against these proinflammatory effects reveals an intricate battle between polyP and APC that is fought on multiple fronts.
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