D. Weiland, H. Hornig-;Do, J. Neuhaus, T. Holzer, C.M. Niessen, D. Tobin, B. Brachvogel, R. Wiesner, O. Baris


Chronic tissue inflammation, a hallmark of aging, is thought to originate from multiple sources, ultimately leading to the secretion of pro-inflammatory cytokines. In recent years, deletions of mitochondrial DNA (mtDNA), which accumulate during aging, have been discussed as potential causes for inflammation. To study if mtDNA alterations and respiratory chain dysfunction could be involved in tissue inflammation in vivo, we have established a mouse model which expresses a severe dominant negative mutation of the mitochondrial helicase TWINKLE (K320E-Twinkle) in epidermal progenitor/stem cells (keratin 14 positive, K320E-TwinkleEpi mice).