Figure 1.

Pathways underlying diabetic neuropathy at the cellular level with corresponding pathogenesis‐derived therapies. Pathogenesis‐derived agents are linked to these pathways by the green boxes and the red lines terminating in a crossbar (indicate blocking of the corresponding pathways). Asterisks indicate randomized placebo‐controlled clinical trials of diabetic sensorimotor polyneuropathy as yet not available. AGEs, advanced glycation end‐products; AMPK, 59 adenosine monophosphate‐activated protein kinase; BiP, binding immunoglobulin protein; CHOP, CCAAT/enhancer‐binding protein homologous protein; CR, cytokine receptor; DNA, deoxyribonucleic acid; ER, endoplasmic reticulum; FFA, free fatty acid; G6P, glucose‐6‐phosphate; GLP‐1 RA, glucagon‐like peptide‐1 receptor agonist; GLUT, glucose transporter; IKK, IκB kinase; IL, interleukin; IR, insulin receptor; JNK, c‐Jun N‐terminal kinase; NAD+, oxidized nicotinamide adenine dinucleotide; RAGE, receptor of advanced glycation end‐products; ROS, reactive oxygen species; TLR, Toll‐like receptor; TNFα, tumor necrosis factor‐α; UPR, unfolded protein response. Reproduced with permission from Bönhof et al., Endocrine Reviews, 2019 ²⁶ . Copyright and all rights reserved.