Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5588235 | Journal of Diabetes and its Complications | 2017 | 19 Pages |
Abstract
Under high glucose conditions mitochondria-mediated oxidative stress and glycation are downstream targets of ins-7. This impairs the neuronal system and longevity via a non-neuronal/neuronal crosstalk by affecting sod-3 and glod-4, thus giving further insight into the pathophysiology of diabetic complications.
Keywords
E. coliC. elegansDAFNACFCCPNGMGFPCTRLLongevityN-acetylcysteineRNA interferenceRNAiROSStandardEscherichia coliInsulin actionforkhead Box Onematode growth mediumSODAgeSuperoxide dismutaseNeuronal functionFoxOMethylglyoxalAdvanced glycation end-productknock-outdiabetic neuropathywild-typearbitrary unitsgreen fluorescent proteinCarbonyl cyanide-4-(trifluoromethoxy)phenylhydrazoneCaenorhabditis elegansControlhigh glucoseReactive oxygen species
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Authors
Michael Mendler, Christin Riedinger, Andrea Schlotterer, Nadine Volk, Thomas Fleming, Stephan Herzig, Peter P. Nawroth, Michael Morcos,