Prof. Isermann elucidated in his talk “Cellular mechanisms: role of mitochondria in the diabetic nephropathy” the evidence of mitochondrial dysfunction in diabetic nephropathy. In a recent human study, genome-wide compartment-specific gene expression profiling and quantitative morphometric analysis of kidney biopsies from 49 Pima Indians with diabetes type 2 and early diabetic kidney disease, showed a link between transcriptional dysregulation and ultrastructural lesions in the diabetic kidney. Tubule-interstitial damage correlated with transcription factors that were enriched for pathways associated with mitochondrial dysfunction. In an experimental mouse model could be already shown in vivo enhanced mitochondrial reactive oxygen species in diabetic nephropathy using a GFP-modified sensor. Although considerate evidence on the mechanisms how hyperglycemia- induced mitochondrial reactive oxygen species participate in the diabetic complications, the translation of this knowledge into therapeutic approaches has failed to show robust responses in delaying or preventing diabetic nephropathy. This might be attributed to the multiple facets of mitochondrial dysfunction in diabetes apart from the production of reactive oxygen species. One important finding in the last years was the functional link observed between mitochondria and endoplasmic reticulum. Moreover, a study from last year showed evidence of fragmented mitochondria in renal tubular injuries in human diabetic nephropathy as well as a correlation between the fragmentation of mitochondria and the tubular damage. Better understanding of the multidimensional role of mitochondria in diabetic late complication could help in the future for the development of novel therapeutics targets.