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. Author manuscript; available in PMC: 2016 Jan 1.
Published in final edited form as: Transplant Rev (Orlando). 2014 Mar 4;29(1):23–32. doi: 10.1016/j.trre.2014.01.002

Fig. 1.

Fig. 1

Intracellular signaling pathways and ionic disturbances engaged during IR injury, resulting in cellular swelling, apoptosis, and necrosis. ADP: adenosine diphosphate; AMP: adenosine monophosphate; AP-1: activator protein-1; ATP: adenosine triphosphate; DAMP: danger-associated molecular pattern; HMGB-1: high mobility group box-1; ICAM-1: intercellular adhesion molecule-1; IL-1: interleukin-1; JNK: c-Jun N-terminal kinase; MAPK: mitogen-activated protein kinase; MPT pore: mitochondrial permeability transition pore; MyD88: myeloid differentiation factor 88; NF-κB: nuclear factor kappa B; RAGE: receptor for advanced gylcation end product; ROS: reactive oxygen species; SOC: store operated calcium channel; TLR: toll-like receptor; TNF: tumor necrosis factor; TRAM: TRIF-related adaptor molecule; TRIF: TIR domain-containing adaptor-inducing interferon; TRP: transient receptor protein; VCAM-1: vascular adhesion molecule-1. Copyright © 2012 Kilian Weigand et al [4]; Open access article distributed under the Creative Commons Attribution License.