Figure 4

Biological model for post-heart transplant survival regulated by the kallikrein-kinin system (KKS). Our predictive analyses converge on a biological role of the Kallikrein-kinin system (KKS) in patient survival post-transplant. Two pathways of the KKS diverge at kininogen (KNG1) transcription into high molecular weight (HK) or low molecular weight (LK) kininogen. LK is cleaved by tissue kallikreins (KLKs) into kallidin and contributes to vasodilation. HK forms a complex with plasma kallikrein and factor 12 to catalyze coagulation. The waterfall cascade involves factor F9 and factor F2 which, in conjunction with fibrinogens, activate fibrin formation. As clotting is upregulated by the increased expression of predictive proteins, the proteinases CPB2 and SERPINF2 inhibit the degradation of clots. Figure made with Biorender.