Pharmacological Protection of Kidney Grafts from Cold Perfusion-Induced Injury
Figure 1
(a) Mechanisms of renal ischemia-reperfusion injury. The main factors contributing to kidney's damage during IRI are oxidative stress and iNOS production, a release of iron ions, accumulation of calcium in the cytosol, mitochondrial uncoupling, and inflammatory immune response. Arrows mark the increase effect (→); dash terminated with line means a decrease (⊢). (b) Potential pathways of the pharmacological protection of kidney graft from ischemia-reperfusion injury. Administration of free radical scavengers, inhibitors of iNOS and MMPs activity, or gasotransmitters are proposed to be a strategy for attenuating renal I/R injury. Yellow mark (x) indicates a potential therapy goal. DGF: delayed graft function; ATP: adenosine triphosphate; MMP-2: matrix metalloproteinase-2; : superoxide radical anion; H2O2: hydrogen peroxide; •HO: hydroxyl radical; OOH: perhydroxyl radical; iNOS: inducible NO synthase; ONOO−: peroxynitrite; NO: nitric oxide.