An mtDNA mutation accelerates liver aging by interfering with the ROS response and mitochondrial life cycle

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• 作者：Jan Niemann^a ; Cindy Johne^a ; Susanne Schrö ; der^a ; Franziska Koch^a ; ^b ; Saleh M. Ibrahim^c ; Julia Schultz^a ; Markus Tiedge^a ; Simone Baltrusch^a ; ^{simone.baltrusch@med.uni-rostock.de}
• 关键词：CAT ; catalase ; COX ; cytochrome c oxidase ; DJ7 ; Parkinson 7 ; DNM1L ; dynamin-1-like protein ; FIS1 ; mitochondrial fission protein 1 ; MFF ; mitochondrial fission factor ; MFN1 ; mitofusin-1 ; MFN2 ; mitofusin-2 ; mtDNA ; mitochondrial DNA ; mtNOD ; C57BL/6NTac-mtNODLtJ ; nDNA ; nuclear DNA ; OPA1 ; optic atrophy 1 ; OXPHOS ; mitochondrial oxidative phosphorylation ; PCX ; pyruvate carboxylase ; PINK1 ; PTEN-induced putative kinase 1 ; ROS ; reactive oxygen species ; SOD1/2 ; superoxide dismutase 1 and 2 ; TFAM ; mitochondri
• 刊名：Free Radical Biology and Medicine
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：102
• 期：Complete
• 页码：174-187
• 全文大小：2677 K
• 卷排序：102

文摘

A COX3 mtDNA mutation affects ROS production and antioxidative response in liver. Old mutant mice show increased metabolism and mitochondrial elongation/clustering. Old control mice show regular metabolism and tend to mitochondrial fragmentation. Liver ballooning degeneration is accelerated in conplastic C57BL/6NTac-mtNODLtJ mice.