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. Author manuscript; available in PMC: 2016 Apr 25.
Published in final edited form as: Biol Chem. 2013 Mar;394(3):319–328. doi: 10.1515/hsz-2012-0316

Figure 1.

Figure 1

Schematic of the eye illustrating the involvement of the components of the KKS in diabetic retinopathy. During the activation of the KKS system, FXII and PPK are proteolytically activated to FXIIa and PK, respectively. PK then cleaves HK to release BK, which can be subsequently cleaved to des-Arg9 BK (DABK). BK and DABK bind to B2R and B1R, respectively, thereby changing retinal vascular permeability, vasodilation, leukostasis, electroretinogram (ERG) activity, and retinal thickness. PK may also contribute to retinal hemorrhage. The activity of PK can be inhibited by C1-INH, PK inhibitor ASP-440, and neutralizing anti-PK antibody. The antagonists of B1R include Des-Arg10 Hoe140, R-954, FOV-2304 and LF22-0542, and an antagonist of B2R is Hoe-140. KKS, kallikrein–kinin system; FXII, factor XII; FXIIa, factor XIIa; PPK, prekallikrein; PK, plasma kallikrein; HK: high molecular weight kininogen; BK: bradykinin; B1R, bradykinin 1 receptor; B2R, bradykinin 2 receptor; C1-INH, C1 inhibitor; DABK: des-Arg9-bradykinin.