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Further, these data were incorporated in the earlier established heme knowledge graph, “HemeKG”, to better comprehend the knowledge surrounding heme biology. Combining hemostasis- and heme-specific terminology, the knowledge available thus far was curated and modeled in a mechanistic interactome. Thus, the computational exploration of the complex network of heme-triggered effects in the blood coagulation system is presented herein.

However, despite several independent reports on these effects, apparently contradictory observations and significant knowledge gaps characterize this relationship, which hampers a complete understanding of heme-driven coagulopathies and the development of suitable and specific treatment options. As such, heme provokes prothrombotic states, either by binding to plasma proteins or through interaction with participating cell types.

Excess labile heme, occurring under hemolytic conditions, displays a versatile modulator in the blood coagulation system.

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